OBJECTIVE:To observe the clinical efficacy and safety of Shuxuetong combined with acupuncture in the treat-ment of patients with stroke during recovery period. METHODS:80 patients with stroke during recovery period were selected and divided into observation group and control group,with 40 cases in each group according to random number table method. Control group received acupuncture,6 times a week. Observation group was additionally given Shuxuetong injection 6 ml added into 0.9% Sodium chloride injection 250 ml,ivgtt,qd,for one month. Clinical efficacy of 2 groups were observed as well as in-tracranial [arteriae cerebri anterior (ACA),middle cerebral artery (MCA),basilar artery (BA)] blood flow rate,neurological deficit score(NIHSS),cognitive ability(MMSE)score,Fugl-Meyer activity score and Fugl-Meyer balance score before and af-ter treatment. The occurrence of ADR was compared. RESULTS:Total effective rate of observation group was 95.0%,which was significantly higher than that of control group(70.0%),with statistical significance(P<0.05). Compared with before treatment, blood flow rate of ACA and MCA were increased significantly in observation group after treatment,and were higher than those of control group with statistical significance (P<0.05). NIHSS,MMSE,Fugl-Meyer activity score and Fugl-Meyer balance score of 2 groups improved significantly after treatment,the observation group was better than the control group,with statistical signifi-cance(P<0.05). No obvious ADR was found in 2 groups. CONCLUSIONS:Shuxuetong combined with acupuncture show signif-icant therapeutic efficacy,and improve intracranial blood flow rate and neurologic function with good safety.

Tetanus is caused by the extremely toxic neurotoxin produced by clostridium tetan i. This toxin shows some similarities with snake venom, both being neur otoxic and having somewhat similar functional groups in their molecular structure and so on. Because of these we decided to use JiDesheng antivenom tablets in the treatm ent of tetanus. Since 1987 we have successfully treated 10 cases of tetanus and ideal results were obtained. This report describes 3 typical cases.

OBJECTIVE: To investigate the effects of exendin-4 on hepatic lipid metabolism, fibrosis and oxidative stress in mice with streptozotocin (STZ)-induced diabetes and explore the underlying mechanisms. METHODS: C57BL/6J mice were fed with high-fat diet (HFD) for 4 weeks and received intraperitoneal injections of 120 mg/kg STZ to induce diabetes. After successful modeling, the mice were randomized into diabetic control group and exendin-4 treatment group (DM+E4), and in the latter group, the mice were given a daily dose of 1 nmol/kg of exendin-4 for 8 weeks. The changes in the body weight (BW) and random blood glucose (RBG) in the mice were recorded. The mRNA expressions of the genes related with liver lipid metabolism, fibrosis and oxidative stress were analyzed using RT-PCR, and the structural changes of the liver tissues were observed with HE, Sirius red and oil red O staining; the expressions of TGF-β1, Nrf2 and HO-1 proteins in the liver tissues were detected using Western blotting. RESULTS: The diabetic mice showed significantly higher RBG levels and BW with obvious lipid deposition, fibrosis and oxidative stress in the liver as compared with the normal control mice ( < 0.001). Exendin-4 treatment of the diabetic mice did not significantly lessened liver lipid deposition but obviously reduced the levels of RBG and TG ( < 0.05), lowered the expression levels of liver fibrosis-related genes TGF-β, -SMA and Col-Ⅰ ( < 0.05), increased the expression levels of the antioxidant genes Nrf2, HO-1 and GPX4 ( < 0.01), and enhanced the protein expressions of Nrf2 and HO-1 in the liver tissues ( < 0.01). CONCLUSIONS Exendin-4 improves liver fibrosis and oxidative stress in diabetic mice by activating Nrf2/HO-1 pathway without significantly reducing liver lipid deposition.
Animals ; Diabetes Mellitus, Experimental ; Exenatide ; Liver ; Liver Cirrhosis ; Mice ; Mice, Inbred C57BL ; NF-E2-Related Factor 2 ; Oxidative Stress ; Streptozocin

Hyperhomocysteinemia (Hhcy) is an independent risk factor for Alzheimer's disease (AD). Visual dysfunction is commonly found and is positively correlated with the severity of cognitive defects in AD patients. Our previous study demonstrated that Hhcy induces memory deficits with AD-like tau and amyloid-β (Aβ) pathologies in the hippocampus, and supplementation with folate and vitamin B12 (FB) prevents the Hhcy-induced AD-like pathologies in the hippocampus. Here, we investigated whether Hhcy also induces AD-like pathologies in the retina and the effects of FB. An Hhcy rat model was produced by vena caudalis injection of homocysteine for 14 days, and the effects of FB were assessed by simultaneous supplementation with FB in drinking water. We found that Hhcy induced vessel damage with Aβ and tau pathologies in the retina, while simultaneous supplementation with FB remarkably attenuated the Hhcy-induced tau hyperphosphorylation at multiple AD-related sites and Aβ accumulation in the retina. The mechanisms involved downregulation of amyloid precursor protein (APP), presenilin-1, beta-site APP-cleaving enzyme 1, and protein phosphatase-2A. Our data suggest that the retina may serve as a window for evaluating the effects of FB on hyperhomocysteinemia-induced Alzheimer-like pathologies.
Alzheimer Disease ; etiology ; metabolism ; pathology ; therapy ; Amyloid beta-Peptides ; metabolism ; Animals ; Dietary Supplements ; Disease Models, Animal ; Folic Acid ; therapeutic use ; Homocysteine ; Hyperhomocysteinemia ; complications ; metabolism ; pathology ; therapy ; Male ; Rats, Sprague-Dawley ; Retina ; metabolism ; pathology ; Retinal Vessels ; metabolism ; pathology ; Vitamin B 12 ; therapeutic use ; tau Proteins ; metabolism