粉防己碱对链脲佐菌素所致糖尿病小鼠海马的保护机制

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Abstract Objective To investigate the protective mechanism of Tetrandrine against hippocampus in Streptozocin(STZ) induced diabetic mice. Methods A total of 32 male C57 mice aged 10-12 weeks were randomly divided into four groups, 8 mice in each group, which were control group, Tetrandrine control group, model group and Tetrandrine treatment group. On the day after the establishment and administration of the diabetic model, the water maze test was used to detect the spatial learning and memory ability of the mice, the enzyme-labeled colorimetric method was used to detect the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) in the homogenate of hippocampus, the enzyme linked immunosorbent assay (ELISA) was used to detect the contents of interleukin-1β (IL-1β), interleukin-6(IL-6) and tumor necrosis factor-α (TNF-α) in hippocampal tissue homogenate. Western blotting was used to detect p-Smad2 and p-Smad3 protein expression of hippocampal tissue. Results Compared with the control group, the spatial learning and memory ability of mice in the model group decreased, and the escape latency of water maze was longer than that in the control group, and the differences were statistically significant (P＜0.05). The SOD content in the hippocampal tissue homogenate of the model group was lower than that of the control group, and the MDA content was higher than that of the control group, the differences were statistically significant (P＜0.05). The contents of IL-1β, IL-6 and TNF-α in the model group were higher than those in the control group, and the differences were statistically significant (P＜0.05). The protein expression levels of p-Smad2 and p-Smad3 in the model group were higher than those in the control group, and the differences were statistically significant (P＜0.05). Compared with the model group, the spatial learning and memory ability of mice in the Tetrandrine treatment group increased, and the escape latency of the water maze was shorter than that in the model group, the differences were statistically significant (P＜0.05). The SOD content in the hippocampal tissue homogenate of the Tetrandrine treatment group was higher than that of the model group, and the MDA content was lower than that of the model group, the differences were statistically significant (P＜0.05). The contents of IL-1β, IL-6 and TNF-α in the Tetrandrine treatment group were lower than those in the model group, and the differences were statistically significant (P＜0.05). The protein expression levels of p-Smad2 and p-Smad3 in the Tetrandrine treatment group were lower than those in the model group, and the differences were statistically significant (P＜0.05). Conclusion Tetrandrine can antagonize hippocampal injury in STZ induced diabetic mice, and its mechanism may be related to inhibition of oxidative stress and its downstream Smad signaling pathway.

Key words： Tetrandrine Streptozocin Diabetes model Hippocampus

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	ZHANG Ru-yi
	LIU Xin
	CAI Fei

Cite this article:

ZHANG Ru-yi,LIU Xin,CAI Fei. Protective mechanism of Tetrandrine against hippocampus in Streptozocin induced diabetic mice[J]. 中国当代医药, 2020, 27(25): 4-8.

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https://www.dangdaiyiyao.com/EN/ OR https://www.dangdaiyiyao.com/EN/Y2020/V27/I25/4

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