TWI692362B - Use of the extract of Eucalyptus lanceolata for preparing a pharmaceutical composition for improving the activity of mitochondria in liver - Google Patents

Abstract

An use of an extraction of emblica officinalis in preparing pharmaceutical composition for repairing liver damage, wherein the pharmaceutical composition including the extraction of emblica officinalis improves the ability of performing the oxidative phosphorylation for the synthesis of the adenosine triphosphate (ATP) by mitochondria in the liver cells which are in contact with the free radicals. The pharmaceutical composition including the extraction of emblica officinalis also reduces the proton leakage of the mitochondria, improves the maximal respiration of the mitochondria, improves the coupling efficiency of the adenosine triphosphate in the mitochondria, improves the spare respiratory capacity of the mitochondria, and reduces the amount of the free radical generated in the liver cells.

Description

The extract of Eucalyptus is used to prepare the medicine group for improving the activity of mitochondria in the liver Use of compound

The present invention relates to the preparation of a pharmaceutical composition for improving the activity of mitochondria in the liver, in particular to the use of an extract of lycopene to prepare a pharmaceutical composition for improving the activity of mitochondria in the liver.

The liver is one of the main metabolic organs in the human body. The liver's work involves metabolizing carbohydrates, proteins and lipids, as well as breaking down, converting and removing toxins from the body. However, during the work of the liver, especially when it decomposes, converts and removes toxins from the body, free radicals are also produced as by-products. Furthermore, for a liver damaged by disease, when the function of the liver is affected by the disease, the amount of free radicals produced by the liver during work also increases.

For liver cells, due to the strong oxidizing power of free radicals, the chance of liver cells exposed to free radicals and the organelles in liver cells being oxidatively damaged is greatly increased. In particular, mitochondria (Mitochondria) act as organelles for oxidative phosphorylation and synthesis of adenosine triphosphate (ATP) in liver cells. When mitochondria are damaged by oxidative damage caused by a large number of free radicals, liver cells cannot be self-active. The mitochondria are fully supplied with energy. In this way, the mitochondria with low activity will have a serious negative impact on the working conditions of the liver cells, and then have a negative impact on the function of the liver.

The present invention provides the use of the extract of lycopene to prepare a pharmaceutical composition that enhances the activity of mitochondria in the liver, thereby enhancing the activity of mitochondria in the liver cells of the liver Maintain the normal function of liver cells.

The present invention discloses the use of an extract of Phyllanthus emblica for the preparation of a pharmaceutical composition that enhances the activity of mitochondria in the liver. The pharmaceutical composition containing the extract of Phyllanthus umbelliferus promotes the oxidation of mitochondria in liver cells in contact with free radicals Phosphorylation reaction and the ability to synthesize linear triglycoside (ATP).

The use of the extract of lycopene according to the present invention as described above for the preparation of a pharmaceutical composition that enhances the activity of mitochondria in the liver. The pharmaceutical composition containing the extract of lycopene enhances the mitochondria of liver cells in contact with free radicals The ability to carry out oxidative phosphorylation and synthesize linear triglycoside (ATP). In this way, mitochondrial activity in hepatocytes is maintained, and mitochondria in hepatocytes can produce sufficient amounts of triglycoside for hepatocytes, thereby maintaining hepatic cells' normal metabolic work. Furthermore, due to the improved efficiency of synthesizing the neurin triphosphate required for repairing cell damage, the damaged liver cells receive sufficient energy for repair.

The above description of the disclosure and the following description of the embodiments are used to demonstrate and explain the spirit and principle of the present invention, and provide a further explanation of the scope of the patent application of the present invention.

FIG. 1 is an infrared absorption spectrum of the Phyllanthus emblica extract used in Examples 1 to 3 of the present invention.

FIG. 2 is a high-performance liquid chromatogram of the extracts of lycopene used in Examples 1 to 3 of the present invention.

FIG. 3 is a schematic diagram of the oxygen consumption of the synthesized neuroside triphosphates according to Examples 1 to 3, Comparative Examples and Control Examples of the present invention.

FIG. 4 is a schematic diagram of oxygen consumption for overcoming hydrogen ion leakage in Examples 1 to 3, Comparative Example and Control Example of the present invention.

FIG. 5 is a schematic diagram of the maximum oxygen consumption capacity of the first to third embodiments, the comparative example and the control example of the present invention.

FIG. 6 is a schematic diagram of the mixing efficiency of Examples 1 to 3, Comparative Example and Control Example of the present invention.

7 is a schematic diagram of the pre-stored oxygen consumption capacity of the first to third embodiments, the comparative example and the control example of the present invention.

8 is a schematic diagram of oleic acid-induced free radical production of liver cells in Example 2, Example 3, Comparative Example and Control Example of the present invention.

The following describes in detail the detailed features and advantages of the present invention in the embodiments. The content is sufficient for any person skilled in the relevant art to understand and implement the technical content of the present invention, and according to the contents disclosed in this specification, the scope of patent application and the drawings Anyone skilled in the relevant art can easily understand the purpose and advantages of the present invention. The following examples further illustrate the views of the present invention in detail, but do not limit the scope of the present invention in any way.

Yuganzi (such as Phyllanthus Emblica or Emblica Officinale), also known as yuzu, oil orange, Amalaka, Malacca (Pokok Melaka), Indian gooseberry (Indian Gooseberry), belongs to the genus Emblica (Emblica) ) The deciduous subarbor is distributed from India to Malaysia and southern China. It is generally considered that India is the origin.

The method for obtaining the extract of the surplus licorice used in the present invention is, for example, using carbon dioxide as a supercritical fluid to extract the surplus of licorice fruit, or methanol, ethanol, acetone, ethyl acetate, a sodium chloride aqueous solution with a concentration of 0.1 to 5% by weight, Potassium chloride aqueous solution, calcium chloride aqueous solution, magnesium chloride aqueous solution or 0.1% to 5% sodium chloride ethanol solution, potassium chloride ethanol solution, calcium chloride ethanol solution, magnesium chloride ethanol solution as the solvent to extract the remaining fruit An initial extract is obtained. Next, the primary extract is filtered and purified to obtain the lycopene extract used in the present invention. The Phyllanthus emblica extract can be spray dried or vacuum dried The drying procedure is carried out to obtain the lycopene extract powder which is easy to preserve.

The edible seed extract contains 35% to 55% by weight of Emblicanin-A and Emblicanin-B mixture, 4% to 15% by weight of Punigluconin, 10% to 20% by weight of Pedunculagin, 5% to 15% by weight Rutin and Gallo-ellagitannoids of 10% to 30% by weight. Amla extract the infrared absorption spectrum to 3403.6 ± 5 cm ^{-1 (cm -1), 2931.6 ±} 5 cm ^{-1 (cm -1), 1385.0 ±} 5 cm ^{-1 (cm -1), 1318.6 ±} 5 cm ^{- 1} (cm ^-1 ), 1623.5±5 cm ^-1 (cm ^-1 ), 1451.3±5 cm ^-1 (cm ^-1 ), 1352.1±5 cm ^-1 (cm ^-1 ), 1218.4±5 cm ^-1 ( cm ^-1 ), 1148.6 ± 5 cm ^-1 (cm ^-1 ), 1035.7 ± 5 cm ^-1 (cm ^-1 ), 3403.6 ± 5 cm ^-1 (cm ^-1 ) have characteristic absorption peaks. The high performance liquid chromatography (HPLC Chromatogram) of Eucalyptus extract has characteristic peak signals at 1.620±0.5 minutes, 2.148±0.5 minutes, 3.265±0.5 minutes and 4.370±0.5 minutes.

The structure of Emblicanin-A (2,3-di-O-galloyl-4,6-(S)-hexahydroxy diphenoyl-2-keto-glucono-lactone) is shown in Formula 1.

The structure of Emblicanin-B (2,3,4,6-bis-(S)-hexahydroxydiphenoyl-2-keto-glucono-lactone) is shown in Formula 2.

Formula two

The structure of Punigluconin (2,3-di-O-galloyl-4,6-(S)-hexahydroxyd iphenoyl gluconic acid) is shown in Formula 3.

The structure of Pedunculagin (2,3,4,6-bis-(S)-hexahydroxydiphenoyl-D-glucose) is shown in Formula 4.

Formula four

The structure of Rutin(3’,4’,5,7-tetrahydroxyflavono-1,3-O-rhamnogl ucoside) is shown in Formula 5.

When an aqueous solution of residual Ganzi extract at a concentration of 100 to 500 micrograms per milliliter (μg/ml) is provided to hepatocytes in contact with free radicals, the residual Ganzi extract entering the liver cells increases the activity of mitochondria in the liver cells. In this way, the number of mitochondria synthesized by oxidized phosphorylation of the mitochondria activated by the extract of Phyllanthus emblica is increased, the maximum oxygen consumption capacity is increased, the pre-existing oxygen consumption capacity is improved, the efficiency of mediated by triglycoside triphosphate and hydrogen Ion leakage is reduced.

Furthermore, when an aqueous solution of residual Ganzi extract at a concentration of 100 to 500 micrograms per milliliter (μg/ml) is provided to liver cells in contact with free radicals, the mitochondria activated by the residual Ganzi extract are synthesized by oxidative phosphorylation. There was no significant decrease in the amount of triglycoside triphosphate, no significant reduction in the efficiency of triglycoside triphosphate mixing, and no significant increase in hydrogen ion leakage. The maximum oxygen consumption capacity of the mitochondria activated by the extract of Phyllanthus emblica slightly increased, and the pre-existing oxygen consumption capacity of the mitochondria slightly increased. Therefore, the extract of Phyllanthus emblica can be used as the active ingredient of a pharmaceutical composition for improving the activity of mitochondria in the liver, and the extract of Phyllanthus uriferae can maintain the activity of mitochondria in liver cells in contact with free radicals Mitochondrial activity in hepatocytes that are not in contact with free radicals. Furthermore, due to the improved efficiency and ability of synthesizing neuroside triphosphate required for repairing cell damage, the damaged liver cells can obtain sufficient energy for repair.

The method for providing the hemp seed extract or the pharmaceutical composition containing the hemp seed extract to the hepatocytes is, for example, ingestion of the hemp seed extract or the medicinal composition containing the hemp seed extract by mouth. When the lycopene extract is provided to the cells in an edible manner, the effective dose of the lycopene extract is 1.081 grams (g) to 5.405 grams (g). The conversion formula is as follows: human effective dose (mg) = effective dose for cell experiments (μg/ml) × mouse body weight (g) × conversion factor × human body weight (kg). The conversion factor is obtained by looking up the conversion factor table of the dose per kilogram body weight of animals and humans. When the mouse weight is 20g and the human body weight is 60kg, the conversion factor is 9.01.

In order to facilitate ingestion of the edible hemp seed extract by oral consumption, the edible hemp seed extract can be made into a processed product of the edible hemp seed extract in, for example, liquid, solid, granular, powder, paste or gel form. The processed products of Ilyxa chinensis extract can be matched with excipients or flavoring agents as additives to enhance flavor and facilitate consumption.

Excipients are, for example, starches such as wheat starch, rice starch, corn starch, potato starch, dextrin, cyclodextrin; crystalline cellulose; lactose, glucose, granulated sugar, reduced maltose, caramel, fructooligosaccharide, emulsified oligosaccharide Sugars such as sorbitol, erythritol, xylitol, lactitol, mannitol, etc.

Flavoring agents are, for example, various fruit juice extracts such as longan extract, litchi extract, grapefruit extract; various fruit juices such as apple juice, orange juice, lemon juice; peach flavor, plum flavor, yogurt flavor and other flavors; acesulfame Various sweeteners such as potassium acid, sucralose, erythritol, oligosaccharides, mannose, xylitol, isomerized sugars; various acidifiers such as citric acid, malic acid, tartaric acid, gluconic acid; green tea, oolong tea, Various tea ingredients such as Banaba Tea, Eucommia tea, Tieguanyin tea, Coix tea, horse chestnut tea, wild white tea, kelp tea; Arabica (Coffee Arabica), Robusta (Coffee Robusta), rely Various coffee ingredients such as Coffee Liberica.

In addition, the edible seed extract or the pharmaceutical composition containing the edible seed extract can also be encapsulated in a capsule to facilitate ingestion of the edible seed extract. The edulis extract or the pharmaceutical composition containing the edulis extract can be coated in hard capsules in the form of dry powder. The edulis extract or the pharmaceutical composition containing the edulis extract can also be coated in soft capsules in the form of solution, suspension, paste, powder or granules.

The fats and oils used in the soft capsules to dissolve or disperse the extracts of lycopene are, for example, calyx pear oil, almond oil, linseed oil, fennel oil, Bai Su oil, olive oil, olive squalene, sweet orange oil, thoracic spine Orange roughy oil, sesame oil, garlic oil, cocoa butter, pumpkin seed oil, chamomile oil, carrot oil, courgette oil, tallow fatty acid, Hawaiian stone fruit oil, lingonberry oil, brown rice germ oil, rice oil, wheat germ Oil, safflower oil, shea butter, liquid shea butter, perilla oil, soybean oil, evening primrose oil, camellia oil, corn oil, rapeseed oil, saw palmetto extract oil, coix oil, Peach kernel oil, parsley oil, castor oil, sunflower oil, grape seed oil, borage oil, Australian walnut oil, meadowfoam oil, cottonseed oil, peanut oil, turtle oil, mink oil, egg butter, Fish oil, palm oil, palm kernel oil, wood wax, coconut oil, long-chain/medium-chain/short-chain fatty acid triglycerides, diglycerides, tallow, lard, squalene, squalane, basking Alkanes, and hydrides of these oils and fats, etc. Among them, borage oil and evening primrose oil contain a large amount of Gamma-Linolenic Acid (GLA). Gamma-Linolenic Acid is an essential fatty acid for the human body. It has moisturizing, cell regeneration and brown fat (Brown Fat) activity Degree to promote the function of fat burning.

In addition, colorants, preservatives, tackifiers, binders, disintegrating agents, dispersing agents, stabilizers, gelling agents, antioxidants, surfactants, preservatives, pH adjusters, etc. are added in compliance with government regulations The product can also be added to the processed products of the edible seed extract in accordance with the dosage standard prescribed by the government unit and the needs of processing and production.

In the following, according to the first to third embodiments of the present invention, the control example and the comparative example The purpose of the present invention is to reveal the use of the extract of the remaining Ganzi for the preparation of a pharmaceutical composition for improving the activity of mitochondria in the liver, and to conduct experimental tests to illustrate that the extract of the remaining Ganzi for the preparation of the present invention is used to improve the liver The efficacy of the use of body-active pharmaceutical compositions.

In the experiment of the present invention, the extract of edulis seeds was used to immerse the fruits of Emblica Officinalis in a 1% by weight aqueous solution of sodium chloride, and then heated in a steam bath at 65°C to 75°C. Hours, followed by filtration, followed by freezing for another 3 days, followed by a spray dry (Spray dry) procedure to obtain a powder of Phyllanthus emblica extract. The dried Phyllanthus emblica extract is in the form of brown powder. The surplus extract contains 27% by weight Emblicanin-A, 23% by weight Emblicanin-B, 8% by weight Punigluconin, 14% by weight Pedunculagin, 10% by weight Rutin and 10% to 30% by weight % Of Gallo-ellagitannoids. The extracts of Phyllanthus emblica in the present invention are not limited to the extracts of Emblica Officinalis . Other extracts of Phyllanthus emblica with different scientific names but similar components also have the same effect.

FIG. 1 is an infrared absorption spectrum of the Phyllanthus emblica extract used in Examples 1 to 3 of the present invention. FIG. 2 is a high-performance liquid chromatography map used in Examples 1 to 3 of the present invention. As shown in Fig. 1, the infrared absorption spectrum of the extract of Eucalyptus lanceolata is at 3403.6 cm ^-1 (cm ^-1 ), 2931.6 cm ^-1 (cm ^-1 ), 1385.0 cm ^-1 (cm ^-1 ), 1318.6 cm ^-1 ( cm ^-1 ), 1623.5 cm ^-1 (cm ^-1 ), 1451.3 cm ^-1 (cm ^-1 ), 1352.1 cm ^-1 (cm ^-1 ), 1218.4 cm ^-1 (cm ^-1 ), 1148.6 cm ^-1 ( cm ^-1 ), 1035.7 cm ^-1 (cm ^-1 ), and 3403.6 cm ^-1 (cm ^-1 ) have characteristic absorption peaks. As shown in FIG. 2, the HPLC Chromatogram of the Phyllanthus emblica extract has characteristic peak signals at 1.620 minutes, 2.148 minutes, 3.265 minutes and 4.370 minutes.

The cells used in the experiment were Hep-G2 cells. The preparation method of the experimental sample is to incubate 24 hours after implanting 20,000 hepatocytes in each well of the 24-well plate. Next, the culture liquid in the well was removed, and then the liver cells in the well were treated according to the conditions of each example, control example, and comparative example.

In the course of the experiment, when preparing the experimental samples of Examples 1 to 3, firstly add the aqueous solution of the extract of the residual Ganzi with a predetermined concentration to the well where the liver cells are located and soak for 24 hours. Next, the aqueous solution in the well where the hepatocytes were located was removed, and a 1.5 mM H ₂ O ₂ aqueous solution was added to the well, and the cells were soaked in the 1.5 mM H ₂ O ₂ aqueous solution for 60 minutes. Then, the H ₂ O ₂ aqueous solution in the well where the hepatocytes are located is removed, and the hepatocytes are washed with phosphate buffered saline (PBS) to complete the preparation of the experimental samples in Examples 1 to 3.

When preparing the experimental sample of the control example, after removing the culture fluid in the well where the hepatocyte is located, the remaining hepatocyte is the experimental sample of the control example. When preparing the experimental sample of the comparative example, first, a 1.5 mM H ₂ O ₂ aqueous solution was added to the wells, and the liver cells were soaked in a 1.5 mM H ₂ O ₂ aqueous solution for 60 minutes. Next, transfer the H ₂ O ₂ aqueous solution in the well where the hepatocytes are located, and wash the cells with phosphate buffered saline (PBS) to complete the preparation of the experimental sample of the comparative example.

In the first embodiment, the concentration of the aqueous solution of lycopene extract is 200 micrograms per milliliter (μg/ml). In the second embodiment, the concentration of the aqueous solution of lycopene extract is 250 micrograms per milliliter (μg/ml). In Example 3, the concentration of the aqueous solution of Ixanthus chinensis extract is 500 micrograms per milliliter (μg/ml).

Next, the oxygen consumption of the hepatocytes in Examples 1 to 3, Control Examples and Comparative Examples in the wells was measured with a hippocampal bioenergy meter. According to the literature, the treatment of cells with hydrogen peroxide can simulate the situation of intracellular oxidation to generate free radicals, thereby studying the mitochondrial activity of cells under oxidative stress. Therefore, after the liver cell lines of Examples 1 to 3 and Comparative Examples were treated with hydrogen peroxide, the oxygen consumption of liver cells was measured with a hippocampal bioenergy meter, and from this, we can understand The effect of the activity of mitochondria.

The measurement principle and process of the hippocampus bioenergy meter are as follows. First, detect the basic oxygen consumption of the cells in the well. Next, add a triphosphate synthase inhibitor to inhibit granules The mitochondria produce mitochondrial triphosphate, and the reduced oxygen consumption at this time is the oxidative phosphorylation reaction of mitochondria to synthesize mitochondrial triphosphate, which is the basic mitochondrial oxygen consumption (Basal Respiration ). The neuraminidine triphosphate synthase inhibitor is, for example, oligomycin (Oligomycin). Next, an appropriate concentration of anti-coupling agent was added to allow the mitochondria to idle in the limit condition without damaging the electron transport chain of the mitochondrial inner membrane to evaluate the maximum mitochondrial oxygen consumption capacity (Maximal Respiration). The anti-coupling agent is, for example, Carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (FCCP). Finally, the addition of electron transport chain inhibitors has completely turned off the mitochondrial oxygen consumption, thereby confirming the measured background value, which is the non-mitochondrial oxygen consumption (Non-mitochondrial Respiration). The electron transport chain inhibitor is, for example, a combination of rotenone and antimycin A.

The basic oxygen consumption of mitochondria is equal to the basic oxygen consumption of cells minus the non-mitochondrial oxygen consumption. The basic oxygen consumption of mitochondria minus the amount of oxygen consumed by synthesizing triglycoside triphosphate is equal to the oxygen consumption to overcome hydrogen ion leakage (Proton Leakage). The maximum mitochondrial oxygen consumption capacity minus the mitochondrial basic oxygen consumption is equal to the mitochondria's stored oxygen consumption capacity (Spare Respiratory Capacity). The Mitochondrial Coupling Efficiency of mitochondrial triphosphate (Coupling Efficiency) is equal to the synthesis of mitochondrial triphosphate oxygen consumption divided by the mitochondrial basal oxygen consumption.

The experimental parameters and experimental measurement results of Examples 1 to 8 and Comparative Examples 1 to 2 and the control example are shown in Table 1 and FIGS. 3 to 7. The experimental measurement results of the picomoles of oxygen consumed per minute (pmol/min/μg protein) per microgram of protein presented in Table 1 are the experimental measurement results after the cell amount has been standardized. FIG. 3 is a schematic diagram of the oxygen consumption of the synthesized neuroside triphosphates according to Examples 1 to 3, Comparative Examples and Control Examples of the present invention. FIG. 4 is a schematic diagram of oxygen consumption for overcoming hydrogen ion leakage in Examples 1 to 3, Comparative Example and Control Example of the present invention. FIG. 5 is a schematic diagram of the maximum oxygen consumption capacity of the first to third embodiments, the comparative example and the control example of the present invention. FIG. 6 is a schematic diagram of the mixing efficiency of Examples 1 to 3, Comparative Example and Control Example of the present invention. 7 is a schematic diagram of the pre-stored oxygen consumption capacity of the first to third embodiments, the comparative example and the control example of the present invention. Figure 8 is the second embodiment of the present invention 3. Schematic diagram of oleic acid-induced liver cell free radical production in Comparative Examples and Control Examples.

As shown in FIG. 3, the oxygen consumption of the synthetic linear triphosphate in Examples 1 to 3 is higher than that of the synthetic linear triphosphate in Comparative Examples. As shown in FIG. 5, the maximum oxygen consumption capacity of the mitochondria of Examples 1 to 3 is higher than that of the comparative example. As shown in FIG. 6, the mixing efficiency of the mitochondria of Examples 1 to 3 is higher than that of the comparative example. As shown in FIG. 7, the pre-stored oxygen consumption capacity of the mitochondria of Examples 1 to 3 is higher than that of the mitochondria of Comparative Example 1. Therefore, from FIGS. 3 and 5 to 7, it can be seen that after the hepatocytes of the first to third embodiments are treated with the extract of edible seed, the activity of mitochondria in the hepatocytes is improved. Furthermore, the increase in the pre-existing oxygen consumption capacity of mitochondria also represents the improvement of the ability of mitochondria and liver cells to respond to various conditions that can cause stress on the cells.

As shown in FIG. 4, the mitochondria of Example 1 to Example 3 have hydrogen ion leakage The amount is lower than that of the mitochondria of the comparative example. Therefore, it can be seen from FIG. 4 that after the hepatocytes of the first to third embodiments are treated with the extract of edible seed, the ability of the mitochondria in the hepatocytes to resist the oxidative damage of free radicals is improved.

Furthermore, as shown in FIGS. 3 to 7, the mitochondria in the hepatocytes of the first to third embodiments are compared with the mitochondria in the hepatocytes of the control example, and the mitochondria are activated by the extract of erythron No significant decrease in the amount of triglycoside triphosphate synthesized by oxidative phosphorylation reaction, no significant reduction in the efficiency of triglycoside triphosphate coordination, and no significant increase in hydrogen ion leakage. The maximum oxygen consumption capacity of the mitochondria activated by the extract of Phyllanthus emblica slightly increased, and the pre-existing oxygen consumption capacity of the mitochondria slightly increased. Therefore, the extract of Eucalyptus can maintain the activity of mitochondria in liver cells exposed to free radicals, close to the activity of mitochondria in liver cells not exposed to free radicals.

Furthermore, as shown in FIG. 3, the oxygen consumption of the synthetic nucleoside triphosphates of Examples 1 to 3 is close to that of the control example, and is significantly higher than that of the comparative example. As shown in FIG. 4, the oxygen consumption to overcome the leakage of hydrogen ions in Examples 1 to 3 is slightly higher than that in the control example, but significantly lower than that in the comparative example. Therefore, from FIGS. 3 and 4, it can be seen that the hydrogen ion leakage of the inner mitochondrial membrane of Examples 1 to 3 is not substantially increased as compared with the hydrogen ion leakage of the inner mitochondrial membrane of the comparative example, which represents the intramitochondrial There was no serious damage to the membrane that caused massive leakage of hydrogen ions. Therefore, the amount of oxygen consumed by the mitochondria to retransport hydrogen ions to the interstitial space of the membrane is reduced, so that the oxygen consumption of synthesizing triglycoside triphosphate and the efficiency of the intermediary of triglycoside triphosphate are close to the control example.

As shown in FIG. 8, based on the amount of free radicals generated in the liver cells of the control example, the free radical generation rate in the liver cells of Example 2 and Example 3 is lower than that of the comparative example Shows that the amount of free radicals produced in the liver cells of Example 2 and Example 3 is lower than that of the liver cells of Comparative Example 1. Therefore, as can be seen from FIG. 8, the higher the concentration of the extract of lycopene provided to liver cells, the better the effect of inhibiting the generation of free radicals in liver cells. The hepatocytes treated with an aqueous solution of lycopene extract at a concentration of 100 to 500 micrograms per milliliter (μg/ml) are protected by the edible seed extract, which reduces the free radicals in the liver cells to the mitochondria in the liver cells The destruction of the membrane. Therefore, the concentration is 100 micrograms per milliliter to 500 micrograms (μg/ml) of the aqueous solution of lycopene extract has the effect of protecting the mitochondria in liver cells. In this way, the time for mitochondria to disintegrate can be delayed, which in turn can delay the occurrence of hepatocyte apoptosis.

The use of the extract of lycopene according to the present invention as described above for the preparation of a pharmaceutical composition that enhances the activity of mitochondria in the liver. The pharmaceutical composition containing the extract of lycopene enhances the mitochondria of liver cells in contact with free radicals The ability to carry out oxidative phosphorylation and synthesize linear triglycoside (ATP). In this way, mitochondrial activity in hepatocytes is maintained, and mitochondria in hepatocytes can produce sufficient amounts of triglycoside for hepatocytes, thereby maintaining hepatic cells' normal metabolic work. Because the efficiency and ability of synthesizing neuroside triphosphate required for repairing cell damage is improved, the damaged liver cells can obtain sufficient energy for repair.

Furthermore, the provision of the extract of edulis seeds to liver cells reduces the damage of free radicals in liver cells to the inner membrane of mitochondria in liver cells. Therefore, the aqueous solution of Eucalyptus extract also has the effect of protecting the mitochondria in liver cells. In this way, the time for mitochondria to disintegrate can be delayed, which in turn can delay the occurrence of hepatocyte apoptosis.

Although the present invention is disclosed as the foregoing embodiments, it is not intended to limit the present invention. The numerical value or numerical range shown in the present invention includes an allowable range that can be understood by those with ordinary knowledge in the field to which the present invention belongs. Without departing from the spirit and scope of the present invention, all modifications and retouching are within the scope of patent protection of the present invention. For the protection scope defined by the present invention, please refer to the attached patent application scope.

Claims (10)

The use of an extract of edulis seeds to prepare a pharmaceutical composition for improving the activity of mitochondria in the liver, wherein: the pharmaceutical composition containing the edulis extracts enhances a plurality of liver cells in contact with free radicals, a plurality of particles The ability of the thread body to carry out the oxidative phosphorylation reaction and the synthesis of triglyceride triphosphate (ATP); wherein the extract of lycopene contains 35% to 55% by weight of Emblicanin-A and Emblicanin-B mixture, and 4% to 4% by weight 15% of Punigluconin, 10% to 20% by weight of Pedunculagin, 5% to 15% by weight of Rutin, and 10% to 30% by weight of Gallo-ellagitannoids; of which the infrared absorption spectrum of the surplus of Gansu extract is 3403.6 ± 5 cm ^{-1 (cm -1), 2931.6 ±} 5 cm ^{-1 (cm -1), 1385.0 ±} 5 cm ^{-1 (cm -1), 1318.6 ±} 5 cm ^-1 (cm ^-1), 1623.5 ± 5 cm ^-1 (cm ^-1 ), 1451.3±5 cm ^-1 (cm ^-1 ), 1352.1±5 cm ^-1 (cm ^-1 ), 1218.4±5 cm ^-1 (cm ^-1 ), 1148.6±5 cm ^-1 (cm ^-1 ), 1035.7 ± 5 cm ^-1 (cm ^-1 ), 3403.6 ± 5 cm ^-1 (cm ^-1 ) have individual characteristic absorption peaks; the high-efficiency liquid phase of the surplus Ganzi extract The chromatogram (HPLC Chromatogram) has a characteristic peak signal at 1.620±0.5 minutes, 2.148±0.5 minutes, 3.265±0.5 minutes and 4.370±0.5 minutes respectively. The use of the edible radix citrifolia extract as described in claim 1 for the preparation of a pharmaceutical composition for enhancing the mitochondrial activity in the liver, wherein the edible radix citrifolia extract is obtained by extracting the fruits of edible oligosaccharides with saline as a solvent. The use of the surplus Ganzi extract as described in claim 1 for preparing a pharmaceutical composition for enhancing mitochondrial activity in the liver, wherein the step of providing the pharmacological composition comprising the surplus Ganzi extract to the liver cells includes edible The pharmaceutical composition. The use of the surplus Ganzi extract as described in claim 1 for preparing a pharmaceutical composition for enhancing mitochondrial activity in the liver, wherein the effective dosage of the surplus Gansu extract is 1.081 grams (g) to 5.405 grams (g). The use of the surplus Ganzi extract as described in claim 4 for preparing a pharmaceutical composition for enhancing the activity of mitochondria in liver, wherein the pharmaceutical composition is coated in a soft capsule or a hard capsule. The use of the surplus Ganzi extract according to any one of claim 1 to claim 5 for preparing a pharmaceutical composition for improving the mitochondrial activity in the liver, wherein the pharmaceutical composition containing the surplus Ganzi extract reduces the Proton leakage of some mitochondria (Proton Leakage). Use of the surplus Ganzi extract according to any one of claim 1 to claim 5 for the preparation of a pharmaceutical composition for enhancing mitochondrial activity in the liver, wherein the pharmaceutical composition containing the surplus Ganzi extract enhances the The maximal respiration of these mitochondria. Use of the surplus Ganzi extract according to any one of claim 1 to claim 5 for the preparation of a pharmaceutical composition for enhancing mitochondrial activity in the liver, wherein the pharmaceutical composition containing the surplus Ganzi extract enhances the Coupling efficiency of these mitochondria. Use of the surplus Ganzi extract according to any one of claim 1 to claim 5 for the preparation of a pharmaceutical composition for enhancing mitochondrial activity in the liver, wherein the pharmaceutical composition containing the surplus Ganzi extract enhances the The pre-stored oxygen consumption capacity (Spare respiratory capacity) of these mitochondria. The use of the surplus Ganzi extract according to any one of claim 1 to claim 5 for preparing a pharmaceutical composition for improving the mitochondrial activity in the liver, wherein the pharmaceutical composition containing the surplus Ganzi extract reduces the The amount of free radicals produced in some liver cells.

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