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OBJECTIVE To investigate the effect and mechanism of Poria cocos polysaccharides on the regulation of blood glucose in type 2 diabetes mellitus （T2DM）model rats by phosphatidylinositol 3-kinase（PI3K）/protein kinase B （Akt）/forked box transcription factor O 1（FoxO1）pathway. METHODS SD rats were randomly divided into blank control group （no modeling ，no administration），model group （modeling，no administration ），metformin group （modeling，200 mg/kg）and P. cocos polysaccharide low-dose，medium-dose and high-dose groups （modeling，100，200，400 mg/kg），8 in each group. Except for blank control group ， other groups were given high fat diet combined with streptozotocin to construct the model of T 2DM rats. At the same time ， administration groups were given relevant dose of medicine intragastrically ，and blank control group and model group were given constant volume of water intragastrically ，once a day ，for consecutive 42 days. During the experiment ，general condition and bodyweight of rats were observed every day ；fasting blood glucose （FBG）of rats were collected ，and oral glucose tolerance test were conducted and area under curve （AUC）was calculated the day before last administration. After last medication ，the heart ，liver， kidney organ index were calculated ；the levels of HbA 1c，TC，TG，MDA，SOD，GSH-Px and hepatic glycogen content were detected. HE staining was used to observe the pathological changes of liver and pancreatic tissue ，and the pathological grade score was calculated. Western blot assay was used to detect the protein expressions of p-PI 3K，p-Akt，p-FoxO1， PEPCK and G 6Pase in liver tissues. RESULTS Compared with blank control group ，the rats of model group suffered cc1965@163.com from polydipsia ，polyphagia and polyuria ；the body weight ， the levels of SOD and GSH-Px ，the protein expressions of p-PI 3K，p-Akt and p-FoxO 1 were significantly decreased （P＜0.05）；liver and kidney organ index ，blood glucose level at 0，0.5 and 2 hours after intragastric administration of glucose solution ，AUC， FBG，HbA1c，serum levels of MDA ，TC，TG and hepatic glycogen content ，liver and pancreatic pathological grade score ，the protein expressions of PEPCK and G 6Pase were all increased significantly （P＜0.05）. Compared with model group ，the general condition of rats in P. cocos polysaccharide groups were all improved ，and all of above indicators had been reversed to varying degrees. CONCLUSIONS P. cocos polysaccharide can downregulate protein expressions of PEPCK and G 6Pase which are key enzymes of gluconeogenesis ，inhibit hepatic gluconeogenesis ，effectively decrease blood glucose levels and regulate glucolipid metabolism in T 2DM model rats by weakening oxidative stress and upregulating PI 3K/Akt/FoxO1 pathway.
ABSTRACT
Professor establishes "scalp acupuncture line" guided by the scalp acupuncture points of international standardization and traditional meridian theory, which can be used to treat tic disorder. With a case, professor 's needling experience for tic disorder is introduced in detail and summarized in order to provide reference for the treatment of the disease.
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Humans , Acupuncture Therapy , Meridians , Tic Disorders , TherapeuticsABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of New Qingkailing injection (NQKLI) on cerebral edema following intracerebral hemorrhage (ICH) induced by collagenase VII in rats.</p><p><b>METHODS</b>After being established into ICH model by collagenase VII, rats were treated with NQKLI by intraperitoneal injection. Forty-eight hrs later, brain contents of water was detected with wet and dry method, calcium content in brain was detected by atomic spectrophotometer, tumor necrosis factor-alpha (TNF-alpha) in brain tissue was determined by liquid competitive ibhibitory immunoassay, and serum matrix metalloproteinase-9 (MMP-9) were detected with enzyme-linked immunosorbent assay (ELISA) respectively.</p><p><b>RESULTS</b>NQKLI reduced the contents of water, calcium and TNF-alpha content of brain tissue and serum MMP-9 in rats with ICH.</p><p><b>CONCLUSION</b>NQKLI could alleviate both vasogenic and cytotoxic cerebral edema by prohibiting calcium over-load, protecting basilar membrane and eliminating inflammation.</p>