corilagin protects non-alcoholic fatty liver disease in mice induced by high fat and high sugar diet via regulating AMPK-autophagy signaling / 中国药理学通报

Aim To explore the effects of corilagin on non-alcoholic fatty liver disease induced by high-fat and high-sugar diet in mice via regulating AMPK-autophagy signaling. Methods Healthy 8-week-old male C57BL/6J mice were randomly divided into control group, model group and corilagin group. The mice of model group and corilagin group were fed with a high-fat and high-sugar diet for four weeks at the age of eight weeks. The corilagin group mice were also intraperitoneally injected with corilagin (20 mg • k g

Effects of tanshinone B regulating LRP6/Wntl/p-catenin pathway on cognitive function of mice with vascular dementia / 中国药理学通报

Aim To explore the protective mechanism of tanshinone B on cognitive dysfunction in mice with vascular dementia.Methods C57BL/6 male mice were divided into control group, vascular dementia model group(VD group), tanshinone B group(TSB 2,4,8 mg·kg-1), donepezil hydrochloride group(1 mg·kg-1), according to the random number table method.The VD model was constructed by the coarctation of bilateral common carotid arteries in mice.Ten days after the successful modeling, the low, medium, and high-dose tanshinone B groups were intraperitoneally injected with tanshinone B, the positive control medicine group was intraperitoneally injected with donepezil hydrochloride, once a day, and the mice in control group and VD group were injected intraperitoneally with the same amount of normal saline for 20 d.Morris water maze test was used to detect the learning and memory ability of mice in each group; the cortex and hippocampus of each group were separated, and MDA, SOD and GSH-Px were determined by spectrophotometry; the pathological changes in the hippocampus of each group were observed by HE staining.The expression of p-LRP6, LRP6, Wnt1 and β-catenin protein in the hippocampus of each group of mice were detected by Western blot.Results Compared with control group, the ability of memory was reduced, the content MDA increased(P<0.01), SOD and GSH-Px activities decreased(P<0.01), and significant pathological damage in hippocampus, the expression of p-LRP6, Wnt1, and β-catenin protein was significantly reduced in VD group(P<0.01).Compared with VD group, the learning and memory abilities of the mice were improved, the content of MDA decreased(P<0.01), the activities of SOD and GSH-Px increased(P<0.01), and the pathological damage in hippocampus was significantly improved.The expression of Wnt1 and β-catenin protein increased significantly in TSB treatment group(P<0.01).Conclusions TSB can improve the cognitive dysfunction of VD mice, and its mechanism may be related to the activation of the LRP6/Wnt1/β-catenin pathway in hippocampus.

Molecular pathologic mechanism associated with ischemic optic neuropathy / 国际眼科杂志(Guoji Yanke Zazhi)

@#Nonarteritic anterior ischemic optic neuropathy(NAION)is caused by ischemia of the short posterior ciliary artery that supplies the lamina area of the optic disc. It usually occurs in over 50-year-old people. It is acute optic neuropathy and featured with acute, monocular, and painless vision loss, which frequently results in severe permanent vision damage and visual field defects. This disease is attracting increased attention of clinical researchers. This paper overviews the current molecular pathology of NAION from these aspects, including pathogenesis, pathological changes, relevant protein molecules and susceptibility genes in previous studies. This paper lays a theoretical foundation for future research on the pathological mechanism and the treatment of NAION.