Rosmarinic Acid Protects Mice from Concanavalin A-Induced Hepatic Injury through AMPK Signaling.

Rosmarinic acid (RA) is extensively utilized in herbal medicine in China. The AMP-activated protein kinase (AMPK) signaling can be activated by RA and inhibited by the synthetic, reversible AMP-competitive inhibitor, Compound C (CC). The objective of this study was to investigate the role of AMPK signaling involving the protective effects of RA on concanavalin A (Con A)-induced autoimmune hepatitis (AIH) in mice. BALB/c mice were treated with RA, with or without CC, followed by the pretreatment with Con A. Analysis of serum aminotransferases and cytokines were conducted and liver tissue histology was performed to evaluate hepatic injury. Cytokine levels in serum and hepatic tissue were respectively measured by enzyme-linked immunoassay (ELISA) and used quantitative (q)PCR. Levels of phosphorylated acetyl CoA carboxylase in the liver, representing AMPK activation, were detected by Western blotting. Compared with the Con A group, serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in RA group (100 and 150 mg/kg/d) were significantly reduced. RA also reduced hepatocyte swelling, cell death, and infiltration of leukocytes in the liver of Con A-treated mice. Serum levels of cytokines, such as interferon-γ (IFN-γ), interleukin-2 (IL-2) and interleukin-1ß (IL-1ß), were reduced by RA pretreatment, while the levels of serum interleukin-10 (IL-10), an anti-inflammatory cytokine, was elevated. These protective effects were reversed by treatment with CC. RA treatment reduced the hepatic damage via the activation of AMPK in the mice of Con A-induced. So RA acts as a potential part in the therapy of autoimmune hepatitis.

Study of the mechanism of anti-ulcer effects of virgin coconut oil on gastric ulcer-induced rat model.

INTRODUCTION: This study aims to evaluate the gastro-protective effects of virgin coconut oil (VCO) on different ulcer models as compared to the standard drug (omeprazole). MATERIAL AND METHODS: Three groups of rats (6 rats per group for each ulcer model) were pre-treated with distilled water for the negative control group, 30 mg/kg of omeprazole for the positive control group and VCO (2 ml per rat) for the treatment group. Animals were pre-treated for 7 days and ulcers were induced with cold restraint stress, piroxicam, ethanol and pylorus ligation. On day eight, animals were sacrificed and ulcer scores were determined based on macroscopic evaluation. The gastric volume, pH, total acidity and mucus content were measured in the pylorus-ligated model. The levels of antioxidants were determined from the gastric tissue homogenates. RESULTS: Virgin coconut oil significantly (p < 0.001) inhibited the ulceration caused by different inducers. The percentage of inhibition for the VCO-treated group was 78.3%, 84.7%, 72.7% and 73.1%, while for the omeprazole-treated group it was 60.8%, 61.5%, 59% and 53.8% in cold restraint stress, ethanol, piroxicam and pylorus-ligated ulcer models, respectively. Virgin coconut oil significantly (p < 0.001) inhibited gastric juice volume and total acidity for VCO and omeprazole treated groups as compared to the non-treated negative control group. Moreover, VCO and omeprazole caused a significant (p < 0.001) increase of gastric mucus content and pH. Virgin coconut oil also proved to have significantly increased glutathione (GSH) and nitrite levels, whereas the levels of SOD, GP, MDA and CAT were significantly (p < 0.001) reduced by VCO relative to the control group. Virgin coconut oil also significantly (p < 0.001) increased the level of prostaglandin in rat tissue homogenate, similar to the omeprazole treated group. CONCLUSIONS: Virgin coconut oil shows a possible association with antioxidant properties to control the regulation of prostaglandin synthesis and protect against reactive oxygen species damage.