Schizandra Protects and Repairs Liver From Alcohol Related Disease lajitgold February 2, 2022
Schizandra Protects and Repairs Liver From Alcohol Related Disease

Discussion: (SC = Schizandra Chenisis)

ALD is a major cause of illness and death. Alcoholic fatty liver is characterized by variable deposition of lipids in the hepatocytes. Fatty degeneration of the liver is induced by the deposition of fat in more than 5% of the hepatocytes. This accumulation of fat in the hepatocytes leads to the development of fatty liver (steatosis), which progresses to hepatitis and fibrosis and finally leads to liver cirrhosis.3

In the present study, we investigated whether SC can protect against fatty liver disease in rats chronically fed ethanol. Our results show that chronic ethanol feeding causes hepatic steatosis as evidenced by elevation of serum ALT and AST, accumulation of hepatic TG and TC, and morphologic changes (small lipid droplets and hydropic degeneration of hepatocytes) in the liver. Importantly, we found that SC administration significantly protects against ethanol-induced fatty liver by reducing elevated serum ALT and AST levels, decreasing lipid levels in the serum and hepatic tissue, and alleviating hepatic lipid accumulation.

SC is a popular herb in traditional oriental medicine; its extracts inhibit preadipocyte differentiation and adipogenesis in cultured cells, leading to decreased body weight and fat tissue mass in high-fat diet-induced obese rats.14 Interestingly, Na et al. have isolated dibenzocylooctadiene lignans from SC, which inhibit FA synthetase.20 The lignans from SC also exert hepatoprotective effects against chronic liver injury in rats.21 Moreover, several recent experimental studies reported its beneficial effect against aging-related liver changes and hepatic hypercholesterolemia.22,23

The accumulation of fat in the liver essentially results from alcohol-induced pathogenic processes, which include an increase in uptake of free FAs, synthesis of free FAs, and a decrease in β-oxidation of free FAs.24 These results demonstrate that ethanol administration increases lipid droplet accumulation in hepatocytes, and significantly increases serum and hepatic TG levels. Feeding the animals SC along with ethanol suppresses the increase of fat accumulation in hepatocytes and hepatocellular ballooning degeneration. In addition, the ethanol-induced increase in TG levels in serum and hepatic tissue was significantly suppressed by SC administration.

It is established that AST can be found in the liver, cardiac muscle, skeletal muscle, kidney, pancreas, leukocytes, and erythrocytes, whereas ALT is present only in the liver.25 Therefore, ALT is a reliable marker for detecting liver injury.26 When a hepatocyte is injured, its plasma membrane is disrupted, leading to the leakage of enzymes into the extracellular fluid, which can then be detected in the serum.27 Increased levels of AST and ALT in the serum, therefore, indicate increased damage and/or necrosis of hepatocytes.28 In this study, we demonstrate that ethanol administration elevates serum AST and ALT levels, whereas SC co-administration significantly decreases the level of these enzymes in the serum, suggesting a decrease in liver cell damage. Therefore, our data show that SC has robust hepatoprotective effects.

Cholesterol is a chemical compound that is a combination of lipid and steroid and is naturally produced by the body. About 80% of the body’s cholesterol is produced by and stored in the liver. The liver is able to regulate cholesterol levels in the blood stream and can secrete cholesterol if it is needed by the body.29 In the present study, we show that chronic ethanol consumption significantly increased serum TC and decreased serum HDL cholesterol levels. However, SC administration resulted in decreased total serum cholesterol levels compared with that of the control (ethanol treated) group. In addition, SC-fed rats showed serum HDL cholesterol levels similar to that of the normal group.

Alcoholic fatty liver is characterized by increased concentrations of TG as a result of impaired FA catabolism due to inhibition of PPARα and due to increased lipogenesis in the liver as a result of activation of the AMPK pathway.30,31 We examined the effect of SC on PPARα gene expression in rat liver tissue. Ethanol administration decreased PPARα gene expression, leading to inhibition of FA oxidation. SC treatment increased the expression of PPARα gene but did not alter PPARγ levels. This suggests that the potential mechanism underlying the protection of ethanol-induced fatty liver by SC likely involves the restoration of PPARα function. Ethanol-induced PPARγ-dependent activation of lipogenesis in the liver is not affected by SC. In addition to PPARα, SREBP-1 plays an important role to activate the genes that encode the enzymes involved in FA synthesis, such as ACC, FAS, and SCD1, and drives the formation of TG.32 In this study, the increased expression of SREBP-1 in ethanol-exposed rats was significantly inhibited by SC treatment, indicating that the protective effects of SC might be related with the modulation of SREBP-1.

Next, we investigated whether SC affects the AMPK signaling pathway to inhibit fatty liver formation in ethanol-fed rats. AMPK is known to play a major role in glucose regulation and lipid metabolism and in controlling metabolic disorders such as diabetes, obesity, and liver hepatitis.7 This study shows that SC treatment results in increased AMPK phosphorylation, which occurs at a much lower level in chronic ethanol-induced liver. This is consistent with the observation that dysregulation of hepatic AMPK signaling in response to chronic ethanol exposure is a crucial mechanism for the development of alcoholic fatty liver. Once activated, AMPK stimulates ATP-generating cellular events, such as glucose uptake and lipid oxidation, to produce energy, while turning off energy-consuming processes, such as glucose and lipid production, to restore energy balance.33 The ethanol-mediated inhibition of AMPK was associated with enhanced ACC activity, increased malonyl-CoA concentrations, and the development of liver steatosis. Altogether, our data indicate that ethanol-induced lipid accumulation and development of fatty liver is reversed by SC via activation of AMPK.

In the present study, we demonstrated that ethanol administration results in an increase in intracellular lipid accumulation in hepatocytes along with increased serum TG content. Histopathological examination of the liver from the animals demonstrated that the number of fatty hepatocytes was significantly increased upon chronic alcohol consumption but returned to normal levels in animals that were also administered SC. These results demonstrate that the alcohol-induced hepatic pathological changes were significantly inhibited in SC-fed rats. Taken together, SC treatment suppresses the increase of lipid accumulation in hepatocytes and hepatocellular ballooning degeneration in the liver. Moreover, treatment of rats with SC for 5 weeks reverses fatty liver to the normal condition, as determined biochemically and histologically.

Therefore, the present study strongly indicates that SC has protective effects against alcohol-induced fatty liver in rats. The cellular mechanisms behind ALD involve close associations of PPARα, SREBP-1, and AMPK and the potential development of steatosis in the liver, but this was mitigated by SC. In conclusion, administration of SC diminishes the accumulation of alcohol-derived lipids in the liver. These results suggest that administration of SC may be useful in preventing and improving fatty liver induced by alcohol.

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