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目的 :探讨氯化甲基汞 (MMC)对发育脑组织损伤的机理。方法 :将 Wistar系妊娠大鼠于妊娠 7～ 1 0 d连续灌胃给予 MMC 4mg/kg,取 P1 (postnatal day 1 ) ,3,5,7,1 0 ,1 5仔鼠脑组织制备常规组织切片 ,采用免疫组织化学法检测 c- Jun表达。结果 :对照组发育阶段仔鼠大、小脑有c- Jun表达。随着出生后时间延长 ,大、小脑c- Jun阳性细胞数下降 ,并且 c- Jun阳性细胞具有典型凋亡形态。实验组 c- Jun表达有高于对照组的趋势 ,其中 P7,1 0 ,1 5小脑中 c- Jun表达明显高于对照组 (P<0 .0 5)。结论 :c- Jun参与了脑细胞发育中正常的凋亡过程。MMC诱导大鼠脑发育中神经细胞凋亡 ,可能是通过 c- Jun表达实现的。
Objective: To investigate the mechanism of methylmercury chloride (MMC) on the development of brain injury. Methods: Wistar pregnant rats were given intragastric administration of 4 mg / kg MMC on day 7 to day 10, and postnatal day 1, 3, 5, 7, 10 and 15 offspring were used to prepare normal tissues The sections were stained and the expression of c-Jun was detected by immunohistochemistry. Results: In the control group, c-Jun expression was observed in the large and cerebellum of the offspring. With the prolonged time after birth, the number of c-Jun positive cells in the cerebellum and cerebellum decreased, and the c-Jun positive cells had the typical apoptotic morphology. The expression of c-Jun in experimental group was higher than that in control group, and the expression of c-Jun in P7, l0, l5 cerebellum was significantly higher than that in control group (P <0.05). Conclusion: c-Jun is involved in the normal apoptotic process in brain cell development. MMC induces neuronal apoptosis during brain development in rats, possibly through c-Jun expression.