AIM To study the inhibitory effect of the cytotoxin (CTX) from guangxi cobra venom on human nasopharyngeal cancer cell (CNE) and other tumons cells. METHODS The cytotoxin was isolated and purified from Guangxi cobra venom by successive chromatography on Sephadex G-50 and CM Sepharose CL-6B columns. Its cytotoxic effects and does-effect relationship on human tumors cell lines were examined by MTT assay. RESULTS The inhibitory effects of CTX CM-5 on CNE, human ovarian carcinoma cell (Ho8990), uterus cervical carcinoma cell (HELA) and lymphoma (YAC) cell lines showed a definite does-effect relationship. The IC 50 (48 h in cubation) was 1.84, 2.59, 1.84 and 0.75 mg?L -1 respctively. The inhibitory effects of CTX CM-5 on CNE increased with time. The IC 50 (3 h and 24 h cubation) was 4.78 and 1.04 mg?L -1 respctively. CONCLUSION CTX from Guangxi cobra venom exhibites strong suppressive effect on cultured tumor cells line in vitro.

Objective:To analyze the effect of depressive state on Alzheimer's disease(AD)mice,3xTg-AD mice were stimulated with chronic social frustration stress(CSDS)and chronic mild unpredictable stress(CUMS),to estab-lish an early AD-induced depression mouse model,and to detect cognitive and behavioral changes,activation of micro-glia in the hippocampus and neuronal loss.Methods:Three-month-old mice were subjected to 8-day stress stimulation alternately,the depressive state of the mice was evaluated by behavior,the evaluation criteria were formulated,and the cognitive behavior was detected and analyzed,and the hippocampal brain tissue sections were stained with immunofluo-rescence to observe the deposition of β-amyloid(Aβ)and the aggregation of microtubule-associated protein(tau),mi-croglia activation and neuronal loss.Results:Depression-related behavioral results showed that the CSDS+CUMS group had depression-related phenotypes.Cognitive-behavioral testing showed that the new object recognition index of the mice in the CSDS+CUMS group was significantly reduced(P＜0.05),and the Morris water maze showed that the spatial memory ability of the CSDS+CUMS group was significantly reduced(P＜0.05),but there was no obvious fear memory loss in the CSDS+CUMS group in the conditioned fear experiment.The results of immunofluorescence staining showed that Aβ deposition appeared in the hippocampus at 4 months of age,the activated microglia increased(P＜0.001),and a certain degree of neuronal loss appeared in the CSDS+CUMS group(P＜0.001);At 8 months of age,the CSDS+CUMS group showed tau protein aggregation early.Conclusion:We established a model of AD-induced de-pression in AD mice,in which 3xTg-AD mice experienced early decline in learning memory and increased AD-related pathological deposition of neurons in the hippocampus,accompanied by microglial activation and neuronal loss.