A mixture of mulberry and silk amino acids protected against D-galactosamine induced acute liver damage by attenuating oxidative stress and inflammation in HepG2 cells and rats.

The liver is an important organ for the removal of toxins and utilization of nutrients. The present study then investigated whether a mixture of mulberry water extracts and silk amino acids protected against acute liver damage in rats induced by intraperitoneal injection of D-galactosamine and the action mechanism. D-galactosamine injection is widely used to develop experimental animal models of acute hepatic disease. In the present study, male Sprague-Dawley rats received intraperitoneal injection of D-galactosamine followed by 200 and 600 mg/kg body weight (BW) of mulberry extracts and silk amino acids (1:3, w/w; MS1:3-L and MS1:3-H), the same amounts of MS with different ratios (1:5, w/w; MS1:5-L and MS1:5-H), and 600 mg/kg bw cellulose (control) for 1 week. The normal-control group received an injection of saline instead of D-galactosamine with the same diet as the control group. D-galactosamine injection (control rats) increased serum ALT, AST and γ-GPT levels, indicating the induction of acute liver damage. The control rats also exhibited reduced glycogen depositions, which contributed to increasing fat synthesis from glucose and elevated serum triglyceride levels. Oxidative stress and inflammation in the liver of the control increased in response to the decreasing antioxidant activity and mRNA expression and increasing TNF-α expression, respectively. Both MS1:3 and MS1:5 reduced serum ALT, AST and γ-GPT levels to ameliorate liver damage. MS1:3 reduced oxidative stress by increasing the activity and expression of antioxidant enzymes, whereas MS1:5 decreased the expression TNF-α in the liver. MS1:3 and MS1:5 improved the necrosis of hepatocytes in H&E staining, which was associated with increased glycogen deposition in PAS staining. MS1:5 had better effects on glycogen accumulation. In conclusion, MS1:3 and MS1:5 can be used as therapeutic agents for acute liver damage.