CN113559144A - Application of glycyrrhiza glabra crude extract in treating non-alcoholic fatty liver disease - Google Patents
Application of glycyrrhiza glabra crude extract in treating non-alcoholic fatty liver disease Download PDFInfo
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Abstract
The invention discloses an application of glycyrrhiza glabra crude extract in treating non-alcoholic fatty liver diseases. The crude extract of Glycyrrhiza glabra Linne is obtained by extracting Glycyrrhiza glabra Linne powder with methanol as solvent under ultrasound, and can be used for treating liver cell lipid accumulation model and non-alcoholic fatty liver disease mouse model. Experimental results show that the glycyrrhiza glabra crude extract can inhibit the accumulation of lipid in HepG2 and AML12 cells, relieve the lipid accumulation condition in the liver of a NAFLD mouse, reduce the MDA content in the liver, increase the GSH content, reduce the ROS content in serum, increase SOD content and improve the oxidation resistance of the mouse. Experiments prove that the glycyrrhiza glabra crude extract has good treatment effect on a liver cell lipid accumulation model induced by oleic acid and palmitic acid and a non-alcoholic fatty liver disease mouse model induced by tyloxapol. The glycyrrhiza glabra crude extract has obvious curative effect on NAFLD and small toxic and side effect, has important significance for developing new medicines and has wide medical application prospect.
Description
Technical Field
The invention relates to the field of biological medicines, in particular to application of a glycyrrhiza glabra crude extract in treating non-alcoholic fatty liver diseases.
Background
Nonalcoholic fatty liver disease (NAFLD) is a clinical pathological syndrome characterized by steatosis and fat storage in liver parenchymal cells without history of excessive alcohol consumption. The progression of the disease course is different, including simple fatty liver, steatohepatitis (NASH), steatohepatitis fibrosis and cirrhosis. The Dionysos study reports for the first time that NAFLD has a global prevalence estimate of 24% to 25% of the general population. NAFLD is closely related to insulin resistance, type 2 diabetes, and arteriosclerotic cardiovascular and cerebrovascular diseases. It is currently believed that the pathogenesis of NAFLD includes mainly "one stroke" dominated by Insulin Resistance (IR) and "a second stroke" dominated by oxidative stress, massive hepatocyte death and fibrosis. The Reactive Oxygen Species (ROS) play an important role in the whole process, as Free Fatty Acids (FFA) are greatly increased, the liver cells are subjected to fatty degeneration to generate a large amount of ROS, the scavenging capability of an organism antioxidant system is exceeded, oxygen stress and a large amount of peroxidation products are generated, proteins and nucleic acids are damaged, the liver cells are damaged, a large amount of liver cells are killed in secondary striking, the autoimmune system is stimulated, the liver bank Pfferson cells are activated, and fibrosis is promoted to occur. NAFLD occurs as a result of an imbalance between pro-and anti-steatosis, pro-and anti-inflammatory.
At present, the basic detection indexes of NAFLD include the following: (1) hepatic lipid metabolism ability: triglyceride (TG) in blood can be used as an index of hepatic lipid metabolism disorder; (2) liver antioxidant capacity: lipid oxidation end product Malondialdehyde (MDA) affects mitochondrial respiratory chain complex and mitochondrial critical enzyme activity in vitro, and its production can also aggravate membrane damage, so that testing the amount of malondialdehyde can reflect the degree of lipid peroxidation of organisms, and indirectly reflects the degree of cell damage. GSH is the most important anti-oxidative sulfhydryl substance in cells, and plays an important role in anti-oxidation, protein sulfhydryl protection, amino acid transmembrane transport and the like. When NAFLD occurs, liver lipid deposition increases serum free fatty acid, and liver takes more free fatty acid, so that the oxidation compensation speed of mitochondria beta is increased, and the generation of ROS is increased. ROS and other substances generated by fat accumulation can consume antioxidant substances such as superoxide dismutase (SOD). Therefore, the detection and evaluation of SOD are also used as the most common index for human oxidative stress and oxidation resistance.
Currently, the treatment of NAFLD mainly comprises three means of non-drug treatment, drug treatment and operation treatment. Common drug treatments include: (1) insulin sensitizer: the insulin sensitizer can resist one-time shock, improve insulin sensitivity and effectively reduce IR. (2) Antioxidant: oxidative stress and lipid peroxidation are often used as "secondary hits" to accelerate the development of steatohepatitis. Antioxidant drugs that have been widely studied at present are vitamin e (ve), GSH, silymarin, and the like. VE improves liver fibrosis in NASH patients, but long-term administration increases the risk of death. (3) Liver-protecting medicine: ursodeoxycholic acid, and lipid serum capsule. The main functions are protecting liver cells, resisting apoptosis, resisting liver inflammation and fibrosis, effectively preventing NAFLD from developing to NASH and hepatic fibrosis, and reducing incidence of liver diseases such as liver cirrhosis and liver function failure. (4) Lipid-lowering drugs: NAFLD is often accompanied by hyperlipidemia, and lipid-lowering drugs are currently the focus of research for treating NAFLD, but are still controversial. The lipid-lowering drugs commonly used in clinic include phenoxy aromatic acids (fenofibrate), statins (atorvastatin and rosuvastatin), and the like.
The approach of treating NAFLD by using the medicine is developed rapidly, but no medicine with good specificity exists. Compared with western medicines, the natural Chinese herbal medicine has the advantages of multiple target points, less adverse reactions, low price and the like, and has huge development prospect. Researches find that the main chemical components of the glycyrrhiza glabra are triterpenoid saponin compounds (glycyrrhizic acid, isoglycyrrhizic acid and the like) and flavonoid compounds (glycyrrhizic acid, glycyrrhetinic acid, liquiritin, isoliquiritin, licochalcone A, glabridin and the like), and the glycyrrhiza glabra has pharmacological effects of resisting atherosclerosis, regulating blood fat, resisting oxidation, resisting inflammation, inhibiting tyrosinase activity and the like. In clinical application, the glycyrrhizin component in glycyrrhiza glabra has obvious effects of relieving cough and eliminating phlegm, clearing heat and detoxicating, treating ulcer, acute and chronic viral hepatitis and the like. However, the therapeutic effect of the glycyrrhiza glabra crude extract on NAFLD is not reported, so the invention aims to explore the possible potential application value of the glycyrrhiza glabra crude extract.
Disclosure of Invention
The invention discloses application of a glycyrrhiza glabra crude extract in a medicament for treating non-alcoholic fatty liver disease.
Further, the liver cell lipid accumulation model is induced by oleic acid and palmitic acid and treated by using a glycyrrhiza glabra crude extract.
Furthermore, the glycyrrhiza glabra crude extract has the function of reducing the intracellular lipid level of HepG2 and AML 12.
Further, the NAFLD of the invention is caused by tyloxapol and is treated by using crude extract of Glycyrrhiza glabra.
Furthermore, the glycyrrhiza glabra crude extract can relieve the lipid aggregation condition in the liver of a NAFLD mouse.
Furthermore, the glycyrrhiza glabra crude extract has the functions of reducing MDA in liver of NAFLD mouse and increasing GSH.
Furthermore, the glycyrrhiza glabra crude extract can reduce ROS in serum of a NAFLD mouse and increase the level of SOD.
Drawings
FIG. 1 is a graph of oil red O staining of intracellular lipid droplets of HepG2 after treatment of example 4;
FIG. 2 is a graph of the oil red O staining of intracellular lipid droplets of AML12 after treatment in example 4;
FIG. 3 is a graph showing the measurement of TG content in HepG2 cells after the treatment of example 5;
FIG. 4 is a graph showing the measurement of intracellular TG content in AML12 after the treatment of example 5;
FIG. 5 is a graph of oil red O staining of lipid droplets in the liver of mice after treatment of example 7;
FIG. 6 is a graph showing the measurement of TG content in the liver of mice after the treatment of example 8;
FIG. 7 is a graph of MDA content in mouse liver after example 8 treatment;
FIG. 8 is a graph of the determination of GSH content in the liver of mice after treatment in example 8;
FIG. 9 is a graph showing measurement of ROS content in serum of mice after the treatment of example 9;
FIG. 10 is a graph showing the measurement of SOD content in mouse serum after the treatment of example 9;
indicates that as compared to the blank group,*p<0.05，**p<0.01; # denotes that in comparison to the model set,#p<0.05，##p<0.01; abbreviations: TG: triglyceride, MDA: malondialdehyde, GSH: reduced glutathione, ROS: active oxygen, SOD: superoxide dismutase.
Detailed Description
The present invention is further illustrated by the following examples, which do not limit the present invention in any way, and any modifications or changes that can be easily made by a person skilled in the art to the present invention will fall within the scope of the claims of the present invention without departing from the technical solution of the present invention.
Materials:
glycyrrhiza glabra is purchased from Aksu, Xinjiang; oil Red O powder was purchased from Sigma-Aldrich, cat #: 215-295-3; SPF male C57BL/6 mice, 20-22g, provided by Liaoning Biotechnology Limited, laboratory animal production license number: SCXK 2010-0001; tyloxapol is available from Sigama under the commercial product number T0307-10 g; TG, MDA and SOD measurement kits were purchased from Nanjing institute of bioengineering; the GSH content detection kit is purchased from Beijing Solaibao science and technology Limited; the ROS ELISA detection kit is purchased from Jiangsu non-sub-Biotechnology Co.
Example 1: preparation of Glycyrrhiza glabra crude extract (TGGE)
Firstly, extracting effective components: pulverizing Glycyrrhiza glabra Linne raw material, sieving with 40 mesh sieve, extracting with 100% methanol for 1 time, 60min, 50.0 deg.C, material-liquid ratio of 1:40g/ml, and ultrasonic extracting at power of 150W. The supernatant was collected and filtered through filter paper, and the remaining impurities were further filtered through a 0.22 μm filter. And evaporating the obtained filtrate to dryness with a rotary evaporator to obtain an extract.
② using the preparation: dissolving the extract in 75% ethanol to obtain 100mg/ml TGGE, and dissolving in physiological saline to obtain 100mg/ml TGGE.
Example 2: HepG2 cell treatment
Cell culture: HepG2 cells were plated at 1X 10 per well6The density of each cell was plated in 6-well plates in DMEM medium containing 10% FBS and 1% streptomycin at 4.5g/L glucose. They were cultured in a cell culture chamber containing 5% carbon dioxide at 37 ℃. After 12h, the cells were starved for 3h with HepG2 in DMEM medium containing only 4.5g/L glucose;
experiment grouping: TGGE dissolved in 75% alcohol was diluted to a TGGE solution with a concentration of 10mg/ml using PBS. Incubation of HepG2 cells with 7.5, 15ug/ml TGGE for 1h followed by incubation of cells with Oleic Acid (OA) (660. mu.M) + Palmitic Acid (PA) (330. mu.M) for 24 h; the treatment groups were divided into a normal group (DMEM medium), a model group (OA (660. mu.M) + PA (330. mu.M)), a drug control group (15ug/ml TGGE), a low concentration treatment group (7.5ug/ml TGGE + OA (660. mu.M) + PA (330. mu.M)), and a high concentration treatment group (15ug/ml TGGE + OA (660. mu.M) + PA (330. mu.M)).
Example 3: AML12 cell processing
Cell culture: AML12 cells were plated at 1X 10 per well6The density of each cell was plated in 6-well plates in DMEM/F12 medium containing 10% FBS, 1% streptomycin, 1% ITS, and 40ng/L Dexamethane. They were cultured in a cell culture chamber containing 5% carbon dioxide at 37 ℃. After 12h, the culture medium containing DMEM/F12 alone was replaced, and AML12 cells were starved for 3 h;
experiment grouping: incubating AML12 cells with 12.5, 25ug/ml TGGE for 1h and then adding OA (660. mu.M) + PA (330. mu.M) to incubate the cells for 24 h; the group was divided into a normal group (DMEM/F12 medium), a model group (OA (660. mu.M) + PA (330. mu.M)), a drug control group (25ug/ml TGGE), a low concentration treatment group (12.5ug/ml TGGE + OA (660. mu.M) + PA (330. mu.M)), and a high concentration treatment group (25ug/ml TGGE + OA (660. mu.M) + PA (330. mu.M)).
Example 4: HepG2, AML12 cell oil red O staining
The medium was discarded and the cells were washed 2 times with PBS; fixing with 4% paraformaldehyde for 30min, removing the fixing solution, and washing cells with PBS for 2 times; soaking with 60% isopropanol for 2s in advance, and dyeing with 0.5% oil red O staining solution prepared with 60% isopropanol for 30 min; discarding the staining solution, washing the cells with PBS for multiple times until the residual oil red residue is washed; staining the nucleus with hematoxylin for 1-2min, discarding staining solution, and washing the cell with PBS for 3 times; adding ammonia water for 1min, discarding, and adding PBS for use. After mounting, the lipid droplets were observed by an optical microscope at a magnification of 200.
The experimental results are shown in the attached figures 1 and 2. The results of oil red O staining showed that the model group significantly increased the generation of lipid droplets in HepG2, AML12 cells, and that TGGE in the treatment group was effective in reducing lipid droplet accumulation induced by OA (660 μ M) + PA (330 μ M).
Example 5: measurement of TG content in HepG2, AML12 cells
Collecting cells, centrifuging at 1000rpm for 10min, removing supernatant, washing cell precipitate with PBS, centrifuging at 1000rpm for 10min, removing supernatant, and leaving cell precipitate; adding PBS, and rapidly and repeatedly freezing and thawing the cells for 6 times by using liquid nitrogen to break the cells; the absorbance was measured by microplate reader colorimetry, as determined by kit manufacturer's instructions.
The TG content is shown in figures 3 and 4. The results showed that OA (660 μ M) + PA (330 μ M) significantly increased TG levels in HepG2, AML12 cells compared to the normal group. Compared with the model group, the TGGE drug experimental group reduced TG levels in HepG2, AML12 cells (p < 0.01).
Example 6: NAFLD mouse model establishment
The mice are kept in an SPF environment at room temperature and a relative humidity of 40% -80%. Each group of 3 was randomly grouped: normal group (normal saline), model group (500mg/kg Tyloxapol (Tyloxapol)), drug control group (100mg/kg TGGE), low dose treatment group (25mg/kg TGGE +500mg/kg Tyloxapol), medium dose treatment group (50mg/kg TGGE +500mg/kg Tyloxapol), high dose treatment group (100mg/kg TGGE +500mg/kg Tyloxapol), drug positive control group (100mg/kg Fenofibrate (Fenofibrate) +500mg/kg Tyloxapol). Intraperitoneal injection with TGGE lasted 7 days, mice were fasted for 12h before the last day of experiment, and mice were intraperitoneally injected with Tyloxapol 1h after intraperitoneal injection of TGGE. Mice were sacrificed 12h before blood and liver sampling.
Example 7: mouse hepatocyte oil red O staining
Mouse liver is adopted, 4% paraformaldehyde solution is fixed for 4 hours and then transferred into 200g/L sucrose-PB solution for dehydration, 300g/L sucrose-PB solution is replaced after 24 hours, tissues are placed in embedding agent after 24 hours, liver tissue slices are placed for 20min at room temperature for natural drying, and oil red O staining as in example 4 is carried out after water vapor on the glass slide disappears.
The experimental results are shown in figure 5, Tyloxapol can obviously increase the lipid accumulation of mouse liver cells, and compared with the model group, TGGE in the treatment group can remarkably relieve the lipid accumulation of mouse liver cells induced by Tyloxapol in a dose-dependent manner.
Example 8: determination of TG, MDA and GSH contents in mouse liver
Taking mouse liver, and weighing (g): volume (ml) ═ 1: 9, adding 9 times of physiological saline, mechanically homogenizing, centrifuging at 2500rpm for 10min, and taking supernatant to obtain TG content to be detected; according to the weight (g): volume (ml) ═ 1: 20, adding 20 times of normal saline, mechanically homogenizing, and measuring the MDA content; according to the weight (g): volume (ml) ═ 1: 10, adding 10 times of GSH reagent I, fully grinding at 4 ℃, and centrifuging at 8000g and 4 ℃ for 10 min; taking supernatant to be tested for GSH content; according to the instruction, detecting the contents of TG, MDA and GSH in the liver of the mouse by using TG, MDA and GSH test boxes, and determining the absorbance value of each hole by using an enzyme-labeling instrument;
the experimental results are shown in figures 6, 7 and 8. The results show that Tyloxapol at a concentration of 500mg/kg significantly increases TG content, MDA content and GSH content in mouse liver (p <0.01) compared to the blank group. Compared with the model group, the low, medium and high dose groups TGGE can obviously reduce the content of TG and MDA in the liver of the mouse and obviously increase the content of GSH in the liver of the mouse (p is less than 0.01). TGGE was more effective than Fenofibrate in alleviating TG and MDA levels in the liver of mice.
Example 9: determination of ROS and SOD content in mouse serum
Collecting blood by eyeball, standing at room temperature, centrifuging at 3000rpm for 5min after serum is separated out, and sucking upper layer serum; according to the specification, detecting the content of each index in the serum of the mouse by using an ROS (reactive oxygen species) and SOD (superoxide dismutase) test box, and measuring the absorbance value of each hole by using an enzyme-labeling instrument;
the experimental results are shown in figures 9 and 10. The results show that Tyloxapol can increase the ROS content in mouse serum (p <0.05) and significantly reduce the SOD content in mouse serum (p <0.01) compared to the blank group. Compared with the model group, the low-dosage group TGGE and the high-dosage group TGGE can both obviously reduce the ROS content in the serum of the mice (p is less than 0.05), and the high-dosage group TGGE can obviously adjust the SOD level in the serum of the mice (p is less than 0.05).
Multiple comparisons and statistical significance were performed between different groups using one-way anova. Statistical analysis was performed using GraphPad Prism 9.0.
Claims (7)
1. Application of Glycyrrhiza glabra crude extract in treating non-alcoholic fatty liver disease is provided.
2. Use according to claim 1, characterized in that: the liver cell lipid accumulation model is induced by oleic acid and palmitic acid and is treated by using a glycyrrhiza glabra crude extract.
3. Use according to claim 1, characterized in that: the glycyrrhiza glabra crude extract has the function of reducing the intracellular lipid level of HepG2 and AML 12.
4. Use according to claim 1, characterized in that: the NAFLD is caused by tyloxapol and is treated by using crude extract of Glycyrrhiza glabra.
5. Use according to claim 1, characterized in that: the glycyrrhiza glabra crude extract can relieve lipid aggregation in liver of NAFLD mice.
6. Use according to claim 1, characterized in that: the glycyrrhiza glabra crude extract has the functions of reducing MDA in the liver of a NAFLD mouse and increasing GSH.
7. Use according to claim 1, characterized in that: the glycyrrhiza glabra crude extract can reduce ROS in serum of a NAFLD mouse and increase the level of SOD.
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| CN116549435A (en) * | 2023-04-28 | 2023-08-08 | 中山大学附属第三医院 | Endoplasmic reticulum stress inhibitor and application thereof |
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| CN116549435A (en) * | 2023-04-28 | 2023-08-08 | 中山大学附属第三医院 | Endoplasmic reticulum stress inhibitor and application thereof |
| CN116549435B (en) * | 2023-04-28 | 2024-04-09 | 中山大学附属第三医院 | Endoplasmic reticulum stress inhibitor and application thereof |
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