Three new anthraquinone derivatives isolated from Symplocos racemosa and their antibiofilm activity / 中国天然药物

Three new alkyl substituted anthraquinone derivatives, trivially named as symploquinones A-C (Compounds 1-3) were isolated from Symplocos racemosa. The structures of these compounds were determined on the basis of extensive spectroscopic analyses (UV, IR, Mass, H- and C-NMR, and two-dimensional (2D) NMR techniques). The resulting data were also compared with the reported literature. These compounds were then subjected to antibacterial or antibiofilm testing. Compounds 1 and 3 exhibited good antibacterial activity in the concentration range of 160-83 μg·mL against Streptococcus mutans, methicillin resistant Staphylococcus aureus and Proteus mirabilis. Both compounds were further screened for anti-biofilm activity, which revealed promising activities at sub-MIC concentrations. None of the compounds were found to be active against Klebsiella pneumoniae.

Hypolipidemic and antioxidant activity of ethanolic extract of Symplocos racemosa Roxb. in hyperlipidemic rats: An evidence of participation of oxidative stress in hyperlipidemia.

Hypolipidemic and antioxidant activity profiles of ethanolic extracts of Symplocos racemosa (EESR) were studied by triton-WR1339 (acute) and high fat diet induced (chronic) hyperlipidemic rat models. In both the models, a significant increase in total cholesterol (TC), triglycerides (TG), very low density lipoproteins (VLDL), low density lipoproteins (LDL) and decrease in high density lipoproteins (HDL) in serum were observed. EESR (200 and 400 mg/kg) and simvastatin (10 mg/kg) administered orally reduced the elevated serum lipids (TC, TG, VLDL, LDL), restored the decreased HDL and improved the atherogenic index. In high fat diet induced hyperlipidemic model, EESR treatment prevented the increased formation of malondialdehyde (MDA) in liver, restored the depleted liver antioxidants, glutathione, superoxide dismutase, catalase significantly. The increased liver cholesterol, HMG-CoA reductase activity and body weight of hyperlipidemic rats were significantly reduced by EESR treatment. The EESR inhibited HMG-CoA reductase, a rate limiting enzyme in cholesterol biosynthesis, thereby causing hypolipidemic effects. EESR treatment also improved histoarchitecture of hepatocytes in hyperlipidemic rats. Experimental findings demonstrated anti-hyperlipidemic and antioxidant activity of EESR, which may be directly or indirectly related to its antioxidant activity. The hypolipidemic activity of EESR may be due to the presence of flavonoids phenolic compounds, phenolic glycosides and steroids.

Hepatoprotective activity of Symplocos racemosa bark on carbon tetrachloride-induced hepatic damage in rats.

The present study aims to evaluate the hepatoprotective activity of ethanol extract of Symplocos racemosa (EESR) bark on carbon tetrachloride (CCl4)-induced hepatic damage in rats. CCl4 with olive oil (1 : 1) (0.2 ml/kg, i.p.) was administered for ten days to induce hepatotoxicity. EESR (200 and 400 mg/kg, p.o.) and silymarin (100 mg/kg p.o.) were administered concomitantly for fourteen days. The degree of hepatoprotection was measured using serum transaminases (AST and ALT), alkaline phosphatase, bilirubin, albumin, and total protein levels. Metabolic function of the liver was evaluated by thiopentoneinduced sleeping time. Antioxidant activity was assessed by measuring liver malondialdehyde, glutathione, catalase, and superoxide dismutase levels. Histopathological changes of liver sample were also observed. Significant hepatotoxicity was induced by CCl4 in experimental animals. EESR treatment showed significant dose-dependent restoration of serum enzymes, bilirubin, albumin, total proteins, and antioxidant levels. Improvements in hepatoprotection and morphological and histopathological changes were also observed in the EESR treated rats. It was therefore concluded that EESR bark is an effective hepatoprotective agent in CCl4-induced hepatic damage, and has potential clinical applications for treatment of liver diseases.