【摘要】 目的通过九香虫水提液对染锰雄性SD大鼠进行干预,探究其对大鼠睾丸损伤的抗凋亡作用及其修复机制。方法将50只8周龄的雄性SD大鼠随机分为5组,即空白组、模型组和九香虫低、中、高剂量干预组。模型组和干预组大鼠按照30 mg/(kg·d)腹腔注射氯化锰溶液,连续2周建立生殖损伤模型,空白组腹腔注射生理盐水;造模同时,九香虫低、中、高剂量干预组大鼠分别按照50、100、200 mg/kg灌胃九香虫水提液,连续4周进行干预,空白组和模型组灌胃蒸馏水。利用Western blot和免疫组化技术检测大鼠睾丸凋亡相关基因Bcl-2、Bax、CytC和Cleaved Caspase-3(C-Cas3)的表达情况。结果与空白组相比,模型组大鼠睾丸的BCL-2表达明显减少(P<0.01),而BAX、CYTC、C-CAS3表达明显增多(P<0.01);与模型组相比,部分九香虫干预组大鼠睾丸的BCL-2表达明显增高(P<0.01),而BAX、CYTC和C-CAS3表达明显降低(P<0.01),且呈剂量依赖性。结论九香虫水提液增加Bcl-2表达的同时可抑制Bax和CytC的表达,进而阻止线粒体凋亡信号的传递,且使其下游信号C-Cas3低表达,最终抑制睾丸生精细胞凋亡。更多还原

【Abstract】 Objective To investigate the anti-apoptotic effects and repair mechanism of Coridius chinensis water extract(CcE) on manganese-induced testicular damage in rats.Methods Fifty eight-week-old male SD rats were randomly divided into five groups: control group,model group and low,medium and high doses of CcE treatment group.The control group was administered with intraperitoneal injection of normal saline,the model group and CcE treatment groups were daily administered with intraperitoneal injection of manganese chloride(30 mg/kg) for 2 weeks to establish the model of reproductive injury.At the same time,CcE treatment groups(low,medium and high doses) were intragastrically administered with 50,100,and 200 mg/kg CcE,respectively,for 4 weeks,while the control group and the model group were intragastrically administered distilled water.Western blot assay and immunohistochemistry were used to detect the expression of apoptosis-related genes,such as Bcl-2,Bax,CytC and Cleaved Caspase-3(C-Cas3) in rats.Results The expression of Bcl-2 in the model group was lower than that in the control group,and the expressions of Bax,CytC and C-Cas3 in the model group were higher than those in the control group.The expression of Bcl-2 in CcE treatment group was higher than that in the model group and the expressions of Bax,CytC and C-Cas3 in CcE treatment group were lower than those in the model group.These results indicated that manganese-induced testicular damage was rescued by CcE administration in a dose-dependent manner.Conclusion CcE increases the expression of Bcl-2 and inhibits the expressions of Bax and CytC,then the transmission of mitochondrial apoptosis signal is prevented,and the downstream signal C-Cas3 is lowly expressed,which ultimately inhibits the apoptosis of testicular spermatogenic cells.更多还原