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康尼辛43通过Ca2+依赖PI3K/Akt信号通路预防辐射诱导的肠损伤
Yue Zhu1,2, Jun Dai1, Bin Song3
1Department of Gastroenterology, the Affiliated Jiangyin Hospital of Xuzhou Medical University, Jiangyin 214400, China.
Radiation research
|April 8, 2024
概括
电离辐射降低了连接素43 (Cx43) 的表达,损害了肠道细胞中的间隙结沟通. 恢复Cx43可能会防止辐射引起的肠损伤.
科学领域:
- 细胞生物学 细胞生物学
- 辐射瘤学 辐射瘤学
- 胃肠病学 胃肠病学
背景情况:
- 辐射诱导性肠损伤 (RIID) 是腹腔皮层放射治疗后的一个重大临床挑战.
- 由连接素 (Cxs) 形成的间隙结,对于细胞间通信和组织平衡至关重要.
研究的目的:
- 调查连接素在辐射引起的肠损伤中的作用和表达.
- 阐明RIID中涉及连xin 43 (Cx43) 的潜在分子机制.
主要方法:
- 使用素-AM光探针评估辐射IEC-6细胞中的间隙结点细胞间通信 (GJIC).
- 采用西方涂抹和免疫光学来分析连接素表达.
- 研究了Cx43沉默对细胞反应和信号通路的影响.
主要成果:
- 照射显著降低了IEC-6细胞中的GJIC,在暴露后24小时效果最为明显.
- 在受辐射的肠道细胞中,连结素43 (Cx43) 的表达显著下降,而其他连结素没有受到影响.
- 通过增加活性氧物种 (ROS),细胞内,细胞毒性和亡,而减少扩散,Cx43敲击加剧了RIID.
- Cx43沉默改变的γ-H2AX和PI3K/AKT通路蛋白水平.
结论:
- 电离辐射降低了Cx43的表达,损害了GJIC并导致肠道损伤.
- Cx43对RIID起着保护作用,可能通过调节PI3K/AKT通路.
- 向Cx43可能为减轻辐射诱导的肠道损伤提供了一个新的治疗策略.
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