Carbon tetrachloride (CCl4)-induced lipid peroxidation associated with hepatic oxidative stress and cell death is an important mechanism of acute liver injury (ALI). Ginsenoside Rd is considered an active ingredient of ginseng. Evidence suggests that ginsenoside Rd may improve ischaemic stroke, nerve damage, cancer and other diseases involving apoptosis, inflammation, oxidative stress, mitochondrial injury and autophagy. However, the effects of ginsenoside Rd on CCl4-induced ALI and its underlying mechanisms are still unclear. In this study, 0.25% CCl4 was injected intraperitoneally in mice to establish a CCl4-induced ALI model. In the Rd treatment group, Rd (10, 20[Formula: see text]mg/kg) doses were injected intraperitoneally 1[Formula: see text]h before and 23[Formula: see text]h after CCl4 administration. Ferroptosis inducer imidazole ketone erastin (IKE) was injected intraperitoneally 4[Formula: see text]h before CCl4 administration to explore the mechanism. The blood and liver were collected 24[Formula: see text]h after CCl4 administration to investigate the effect and mechanism of ginsenoside Rd on CCl4-induced ALI. Our results showed that ginsenoside Rd inhibited CCl4-induced ALI in mice. Ginsenoside Rd also downregulated CCl4-induced serum and liver iron, 4-hydroxynonenal, and 8-hydroxy-2 deoxyguanosine levels. Furthermore, it upregulated glutathione and glutathione peroxidase 4 levels. In addition, ginsenoside Rd downregulated the expression of cGAS and STING. Subsequently, the ferroptosis inducer imidazole ketone erastin significantly reversed the hepatoprotective effect and influence of ginsenoside Rd with regard to the indicators mentioned above. Our study confirmed that ginsenoside Rd ameliorated CCl4-induced ALI in mice, which was related to the reduction of ferroptosis. Simultaneously, the ginsenoside Rd-mediated inhibition of the cGAS/STING pathway contributed to its antiferroptosis effect. In conclusion, our results suggested that ginsenoside Rd inhibited ferroptosis via the cGAS/STING pathway, thereby protecting mice from CCl4-induced ALI. These results suggested ginsenoside Rd may be used as a potential intervention treatment against CCl4-induced ALI.
Background: Ginsenoside Rc is one of the cardinal bioactive components of Panax ginseng that has been studied for various biological activities. This study aimed to investigate the protective effects of ginsenoside Rc against acute cold exposure induced myocardial injury in rats.Methods: The rats were intragastrically administrated with ginsenoside Rc (10, 20 mg/kg) or vehicle daily for 7 days. One hour after the seventh-day administration, 3% pentobarbital sodium was used to anesthetize the rats. Rats of the control group were kept in room temperature (22 ± 1 ℃) and the other groups of rats were exposed to low ambient temperature (-15 ± 1 ℃) in a cold chamber for 6 h. Cardiac function was monitored and recorded as well. To evaluate the protective effects of ginsenoside Rc, we also measured myocardial specific enzymes (lactate dehydrogenase, aspartate aminotransferase and creatine kinase-MB) in plasma, whole blood viscosity (WBV), plasma viscosity (PV), erythrocyte sedimentation rate (ESR) and hematocrit (HCT). The pathological changes of myocardium were observed through histopathological examination. The mRNA expression levels of TNF-α, IL-1β and IL-6 were by real-time quantitative PCR analysis. And the expressions of silent information regulator1 (SIRT1), B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X (Bax) and Procaspase-3 in heart tissues were measured by Western blot method.Results: Ginsenoside Rc alone had no effect on cardiac function, myocardial enzyme activities and hemorheology in normal rats. Compared with the model group, pretreatment with ginsenoside Rc significantly improved cardiac function, diminished myocardial specific enzymes release and decreased erythrocyte aggregation index. As a result, the pretreatment regulated abnormal hemorheology, attenuated myocardial histological changes and structural abnormalities, reduced the mRNA expression levels of cardiac inflammatory markers. Ginsenoside Rc also resulted in up-regulating SIRT1, Bcl-2 and Procaspase-3 expressions and down-regulating Bax expression.Conclusion: The current study suggests that ginsenoside Rc alleviates acute cold exposure induced myocardial injury in rats by inhibiting cardiomyocyte apoptosis via SIRT1 and reducing inflammatory response.
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