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百草枯诱导肾毒性大鼠中钙结合蛋白免疫反应性的变化。

The changes of calretinin immunoreactivity in paraquat-induced nephrotoxic rats.

机构信息

Korean DNA Repair Research Center, Chosun University, Gwangju, Republic of Korea.

出版信息

Acta Histochem. 2012 Dec;114(8):836-41. doi: 10.1016/j.acthis.2012.02.005. Epub 2012 Mar 30.

Abstract

Calcium-binding proteins are present in the kidneys: calbindin D-28k in the distal tubules and calretinin in the proximal tubules. Since paraquat causes degeneration in the brush border-bearing proximal tubule cells in rat kidneys, we investigated the changes of calretinin immunoreactivity in the proximal tubule cells of paraquat-induced nephrotoxicity in experimental male Sprague-Dawley rats following chitosan oligosaccharide pretreatment to investigate its protective properties. Paraquat (60 mg/kg) was administered intraperitoneally with or without chitosan oligosaccharide (500 mg/kg, p.o.) pretreatment. The changes on calretinin were compared with those of calbindin D-28k by immunohistochemistry and Western Blot analysis. Calretinin was immunolocalized on the apical surface of proximal tubule cells in the deeper cortex of normal kidney, and disappeared after paraquat administration with minor changes of calbindin D-28k immunoreactivity in the distal tubules and collecting ducts. Chitosan oligosaccharide pretreatment caused increased expression of calretinin and calbindin D-28k before paraquat injection and helped preserve proximal tubules after paraquat treatment. However, Western blot analysis on calretinin and calbindin D-28k could not explain the degeneration of the proximal tubule cells in paraquat-induced nephrotoxicity. These findings suggested that calretinin is a possible and more useful histopathological marker for proximal tubule cells in paraquat-induced nephrotoxic rats.

摘要

钙结合蛋白存在于肾脏中

远曲小管中的 calbindin D-28k 和近曲小管中的 calretinin。由于百草枯会导致大鼠肾脏刷状缘带细胞的退化,我们研究了壳寡糖预处理对百草枯诱导的肾毒性实验雄性 Sprague-Dawley 大鼠近曲小管细胞中 calretinin 免疫反应性的变化,以探讨其保护作用。用壳寡糖(500mg/kg,po)预处理或不预处理腹腔注射百草枯(60mg/kg)。通过免疫组织化学和 Western Blot 分析比较 calretinin 的变化与 calbindin D-28k 的变化。calretinin 在正常肾脏深层皮质的近曲小管细胞的顶膜表面免疫定位,百草枯给药后消失,而远曲小管和集合管中的 calbindin D-28k 免疫反应性变化较小。壳寡糖预处理在注射百草枯前引起 calretinin 和 calbindin D-28k 的表达增加,并有助于百草枯治疗后保护近曲小管。然而,calretinin 和 calbindin D-28k 的 Western blot 分析不能解释百草枯诱导的肾毒性中近曲小管细胞的退化。这些发现表明,calretinin 可能是百草枯诱导的肾毒性大鼠近曲小管细胞的一种更有用的组织病理学标志物。

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