The role of SIRT6 in nonalcoholic steatohepatitis / 生理学报

SIRT6, a member of the silencing information regulatory protein family, is a nicotinamide adenine dinucleotide-dependent histone deacetylase and an ADP-ribose transferase enzyme. It plays an important role in fundamental physiological and pathological processes, including lipid metabolism, inflammation, oxidative stress and fibrosis, and is considered as a potential therapeutic target for metabolic syndrome. SIRT6 knockout mice displayed severe fatty liver, and the expression of SIRT6 in the liver of nonalcoholic steatohepatitis (NASH) mice was significantly lower than that of normal mice. Overexpression of SIRT6 significantly ameliorated NASH-induced liver damage. It is suggested that SIRT6 may play a key role in protecting against NASH. In this paper, we review the important regulatory functions of SIRT6 in the occurrence and development of NASH.

Role of HCO3- umbrella in the pathogenesis of primary biliary cholangitis / 临床肝胆病杂志

Primary biliary cholangitis (PBC) is an autoimmune disease. Although PBC has the features of autoimmune disease, it has poor response to immunosuppressants and good response to the drugs participating in bile acid metabolism, such as ursodeoxycholic acid. Studies have shown that the bicarbonate secretion of biliary epithelial cells is impaired in PBC patients, and bile acid not blocked by HCO3- umbrella enters biliary epithelial cells and mediates their damage and apoptosis, leading to the expression of autoantibodies in apoptotic cells and immunologic injury. In order to explore the role of HCO3- umbrella secreted by biliary epithelial cells in the pathogenesis of PBC, this article briefly introduces the physiological function and production mechanism of HCO3- umbrella and the influencing factors for HCO3- secretion, and it is pointed out that reduced HCO3- secretion may be a key link in the pathogenesis of PBC and a potential therapeutic target.

Effects of electroacupuncture on expression of calmodulin in the hippocampus of rats with cerebral ischemia-reperfusion injury / 中国针灸

<p><b>OBJECTIVE</b>To investigate the protective effect of electroacupuncture (EA) on injured neurons and the signal transduction mechanism of calmodulin (CaM) in rats with cerebral ischemia-reperfusion injury (CIRI).</p><p><b>METHODS</b>A total of 25 SD rats were randomly divided into a sham-operation group, a model group, an EA. group, a TFP group and an EA+TFP group. The rat model of middle cerebral artery occlusion (MCAO) was established by the modified Longa thread occlusion method. The EA group was treated with EA at "Dazhui" (GV 14) and "Baihui" (GV 20) for 30 minutes. The TFP group was treated with lumbar intrathecal injection of Trinuoperazine (TFP) at a dose of 40 microL/kg, the inhibitor of CaM. The EA + TFP group was treated with EA combined with TFP, and the sham-operation group and the model group without any treatment. The neurology deficit score was evaluated by the Julio's neuroethology score methods in all rats, and the expression of CaM in cerebral hippocampus tissue was detected with immunohistochemical method in different intervention condition.</p><p><b>RESULTS</b>(1) In comparison with the model group of 6.90 +/- 1.66, the neuroethology score in the EA group of 14.50 +/- 1.08, the TFP group of 11.70 +/- 1.06 and the EA + TFP group of 14.30 +/- 1.06 were all significantly increased (all P < 0.01), while those still were all lower than the sham group of 17.60 +/- 0.52 (all P < 0.01), and the EA group was better than the TFP group (P < 0.01). (2) In comparison with the sham group of 0.080 +/- 0.045, the immune positive expression score of CaM protein in hippocampus in the model group of 1.680 +/- 0.268 was sig nificantly increased (P < 0.01). In comparison with the model group, the expression score of CaM protein in the EA group of 0.880 +/- 0.179, the TFP group of 0.720 +/- 0.179 and the EA + TFP group of 0.420 +/- 0.249 were all significantly reduced (all P < 0.01), and the expression score of CaM in the EA + TFP group was lower than that in the TFP group (P < 0.05).</p><p><b>CONCLUSION</b>EA can reduce the injury of cerebral neurons induced by CIRI in rats and promote the recovery, which may be related to its effect in regulating CaM signaling pathway after the ischemia-reperfusion injury.</p>