Gastrodin improves hippocampal neurogenesis by NO-cGMP-PKG signaling pathway in cerebral ischemic mice / 中国中药杂志

This paper was aimed to investigate the effect of gastrodin( GAS) on hippocampal neurogenesis after cerebral was chemic and to explore its mechanism of action related to NO. The cerebral ischemia model of C57 BL/6 mice was established by bilateral common carotid artery occlusion. The pathological changes in hippocampal CA1 region and the cognitive function of mice were assessed by HE staining and Morris water maze test,respectively. The count of Brd U/Neu N positive cells in dentate gyrus was detected by immunofluorescence assay. The NOS activity and the NO content were determined by colorimetric and nitrate reduction methods,respectively.The level of c GMP was measured by ELISA kit,and the PKG protein expression was tested by Western blot. On postoperative day 8,the hippocampal CA1 pyramidal neurons of mice showed irregular structure,with obvious nuclear pyknosis,loose cell arrangement and obvious decrease in the number of neurons. On postoperative day 29,the spatial learning ability and memory were decreased. These results indicated cerebral ischemia in mice. Meanwhile,the Brd U/Neu N positive cells were increased significantly in ischemic mice,indicating that neurogenesis occurred in hippocampus after cerebral ischemia. Treatment with different doses of gastrodin( 50 and 100 mg·kg-1) significantly ameliorated the pathological damages in the CA1 region,improved the ability of learning and memory,and promoted hippocampal neurogenesis. At the same time,both the NOS activity and the NO concentration were decreased in model group,but the c GMP level was increased,and the PKG protein expression was up-regulated. Gastrodin administration activated the NOS activity,promoted NO production,further increased c GMP level and up-regulated PKG protein expression. These results suggested that gastrodin can promote hippocampal neurogenesis after cerebral ischemia and improve cognitive function in mice,which may be related to the activation of NO-cGMP-PKG signaling pathway.

Effect of liver X receptor activation on hippocampal neural stem cell proliferation and cognitive function in global cerebral ischemia/reperfusion mice / 中国药理学通报

Aim To investigate the effect of liver X receptor (LXR) activation on the proliferation of hippocampal neural stem cells in global cerebral ischemia/reperfusion (I/R) mice,and its mechanisms.Methods A total of 75 C57BL/6 mice were randomly divided into three groups,namely the sham operation group,the cerebral I/R group and the cerebral I/R with TO901317 treatment (I/R + TO90) group.The I/R mouse model was induced via the bilateral common carotid artery occlusion.HE staining was used to detect the pathological changes in hippocampal CA1 region.Immunohistochemistry was executed to detect hippocampus DCX + cells.Immunofluorescence of BrdU was implemented to detect the proliferation neural stem cell.Morris water maze test was used to assess spatial learning and memory in mice.Western blot was used to detect the expression of hippocampus LXRα,LXRβ,ABCA1,p-ERK1/2,t-ERK1/2,p-CREB,t-CREB,BDNF.Results LXR activation improved cognitive recovery(P ＜0.01),and induced the proliferation of neural stem cells (P ＜ 0.01) in I/R mice.The expressions of hippocampal ABCA1,p-ERK1/2,p-CREB,BDNF in I/R + TO90 group mice also increased (P ＜ 0.01).Conclusions LXR activation can induce the proliferation of hippocampal neural stem cells and facilitate cognitive recovery following global cerebral I/R in mice,which may be related to the activation of hippocampal ERK1/2-CREB-BDNF pathway and then promoting endogenous neurogenesis in the hippocampus DG region of I/R mice.

Baicalin suppresses beta-amyloid protein induced hippocampal cyclooxygenase-2 expression / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the brain protection of baicalin on rats with Alzheimer's disease (AD) and its probable mechanism of action.</p><p><b>METHODS</b>Thirty-six male healthy Wistar rats were randomly divided into the sham-operative group, the AD group, and the baicalin group, twelve in each. beta-amyloid protein 1-40 was injected to the bilateral hippocampus of rats in the AD group and the baicalin group to establish the AD rat model. The sham operation was performed to rats of the sham-operative group in the same way. Equal volume of 0.9% sodium chloride solution was injected to the bilateral hippocampus of rats in the sham-operative group. Baicalin was intraperitoneally injected at the daily dose of 40 mg/kg to rats in the baicalin group before and after operation, once daily for 7 successive days. Equal volume of buffer solution was intraperitoneally injected to rats in the sham-operative group and the AD group in the same procedures at the same time points. The expression of hippocampal cyclooxygenase-2 (COX-2) was determined by Western blot. The spatial learning memory capacities was observed using T-morris test. Histological changes were observed using hematoxylin-eosin (HE) staining.</p><p><b>RESULTS</b>Results of the T-morris test showed the spontaneous alternation selective ratio decreased in the AD group (28.33% +/- 7.50%) and the baicalin group (38.33% +/- 7.50%) (both P < 0.05) when compared with the sham-operative group (61.67% +/- 7.50%). There was significant difference between the AD group and the baicalin group (P < 0.05). Results of HE staining showed degeneration and necrosis of cortical and hippocampal neurons in the AD group and the baicalin group. Changes in the AD group were more obvious. Results of Western blot showed the expression of hippocampal cyclooxygenase (COX-2) obviously increased in the AD group, while it obviously decreased in the baicalin group (P < 0.05).</p><p><b>CONCLUSION</b>Baicalin could alleviate beta-amyloid protein induced brain injury, which might be associated with its inhibition on the COX-2 expression.</p>

Application quantitative thermal sensory test in facial palsy / 中华物理医学与康复杂志

Objective To investigate quantitatively the thermal sensation characteristics of the patients with facial palsy and the value of quantitative thermal test (QTT) in prognostication.Methods The QTT threshold of the fore ear and cheek of 30 patients with peripheral facial palsy was tested,their facial nerve conduction velocity was measured,and House-Brackmann facial nerve grading system was used to estimate facial nerve function at 2～3 weeks,a month,two months and half a year post onset.Results It was found that 12 out of 30 patients had abnor- mal QTT threshold value;the majority of them suffered from herpes virus and diabetes.In those with abnormal QTT, 8 were with diabetes mellitus (account for 66.7%),3 with partial shingles (account for 25%),and 1 with positive serum virus infection (account for 8.3%).Those with normal QTT were significantly different from those with abnor- mal QTT,with regard to the House-Brackmann rating scores after 2 and 6 months post onset (P