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作 者:宋来新[1] 张长城[1] 刘静[1] 黄威峰 袁丁[1] 赵海霞[1] SONG Laixin ZHANG Changcheng LIU Jing HUANG Weifeng YUAN Ding ZHAO Haixia(Medical College of China Three Gorges University, Yichang 443002 Hubei, Chin)
出 处:《中药新药与临床药理》2017年第1期46-51,共6页Traditional Chinese Drug Research and Clinical Pharmacology
基 金:国家自然科学基金(81573931;81373881;81503334);三峡大学人才科研启动基金(KJ2014B067)
摘 要:目的探讨五子衍宗方总黄酮(Total flavonoids from Wuzi Yanzong prescription,TFWZ)对环磷酰胺(Cyclophosphamide,CTX)致成年雄性小鼠睾丸生殖细胞凋亡的影响。方法利用腹腔注射CTX制备小鼠少弱精症模型,灌胃给予TFWZ,末次给予CTX 12 h后称体质量处死小鼠,计算睾丸指数和附睾指数;HE染色观察小鼠睾丸组织形态学变化;TUNEL检测小鼠睾丸细胞凋亡的变化;Western blot检测小鼠睾丸细胞内Caspase-3、p-p53和p-p38蛋白的表达情况。结果与模型组比较,TFWZ可显著增加小鼠体质量、睾丸质量、睾丸指数、附睾质量和附睾指数,改善睾丸组织形态,并显著减少睾丸细胞凋亡,降低睾丸内Caspase-3、p-p53和p-p38蛋白的表达。结论 TFWZ能显著减少CTX致小鼠睾丸生殖细胞凋亡,其机制可能与抑制p38活化,减少p53磷酸化有关。Objective To investigate the effects of total flavonoids from Wuzi Yanzong prescription(WYP-TF)on the apoptosis of testicular germ cells in adult male mice induced by cyclophosphamide(CTX),and to explore its possible mechanism. Methods The mice model of oligozoospermia was established by intraperitoneal injection with CTX,and WYP-TF was administered to the mice orally. The mice were sacrificed 12 h after last medication of CTX. The testes were immediately isolated and weighed,and then we calculated the testis index and epididymis index. The pathological changes in the testes were observed by HE staining. The apoptosis of germ cells in the testes was detected by TUNEL.The protein expression levels of Caspase-3,p-p38 and p-p53 were examined by Western blot. Results Compared with the model control group, WYP-TF significantly increased the body weight, testis weight, testis index,epididymis weight and epididymis index,and significantly improved the morphology of the testes. Moreover,WYP-TF significantly inhibited the apoptosis of germ cells,and decreased the protein expression levels of Caspase-3,p-p38 and p-p53 in the testes. Conclusion WYP-TF can effectively reduce the apoptosis of germ cells in the testes of adult male mice induced by CTX through regulating the activation of p38 and phosphorylation of p53.
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