Cadmium‑induced autophagy promotes survival of rat cerebral cortical neurons by activating class III phosphoinositide 3‑kinase/beclin‑1/B‑cell lymphoma 2 signaling pathways
作者： QI-WEN WANG , YI WANG , TAO WANG , KANG-BAO ZHANG , CHENG-YANG JIANG
关键词:
摘要: Autophagy is an evolutionarily conserved response that can be activated in to heavy metal. Thus, the present study investigated effect of autophagy on neurotoxic damage caused by cadmium (Cd) rat cerebral cortical neurons. The results indicated viability neurons treated with Cd was markedly decreased a dose-and time-dependent manner. provided evidence underwent autophagy: conversion microtubule-associated protein 1A/1B-light chain 3 (LC3) LC3-II, increase punctate distribution endogenous LC3-II and presence autophagosomes were identified. Combined treatment chloroquine, inhibitor, reduced amount autophagocytosis cell activity, whereas rapamycin, inducer, Cd-mediated cytotoxicity. Furthermore, it found beclin-1 class III phosphoinositide kinase (PI3K) levels increased, while anti-apoptotic B-cell lymphoma 2 (Bcl-2) after treatment. LY294002, specific inhibitor PI3K, prevented decline Bcl-2 production beclin-1, PI3K following In conclusion, suggested induce cytoprotective activating PI3K/beclin-1/Bcl-2 signaling pathway, pathway serve as sensitive biomarker for nervous system injury exposure Cd.
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