红景天苷可通过抑制线粒体氧化应激减轻模拟失重大鼠脑动脉的炎性反应

李文凡; 曹青林; 李培杰; 卜英睿; 汤海峰; 谢满江

doi:10.12125/j.chj.202102060

红景天苷可通过抑制线粒体氧化应激减轻模拟失重大鼠脑动脉的炎性反应

Salidroside reduces inflammation of cerebral artery in simulated weightlessness rats by inhibiting mitochondrial oxidative stress

摘要

摘要:
目的探讨红景天苷（SAL）是否会通过抑制线粒体的氧化应激，从而恢复模拟失重大鼠脑动脉的炎性反应。
方法利用尾部悬吊方法建立大鼠模拟失重模型，将24只成年雄性Sprague-Dawley 大鼠随机分为4组：对照（CON）组、对照+红景天苷（CON+SAL）组、尾部悬吊（SUS）组和尾部悬吊+红景天苷（SUS +SAL）组，每组6只（n=6）。尾吊1周后，免疫荧光法检测脑动脉内白细胞介素-1β（IL-1β）和线粒体内SOD（SOD2）的荧光强度，实时定量聚合酶链反应（qRT-PCR）检测脑动脉内白细胞介素-1β（IL-1β）的mRNA水平变化，免疫印迹法（Western Blot）检测脑动脉内白细胞介素-1β（IL-1β）和脑动脉线粒体内超氧化物歧化酶（SOD2）的蛋白表达，共聚焦显微镜下观测MitoSOX染色的急性分离脑动脉平滑肌细胞线粒体内活性氧（ROS）含量。
结果与CON组相比，SUS组脑动脉中IL-1β染色荧光强度和蛋白表达显著增加（均P<0.01），mRNA水平增加（P<0.05），提示SUS可导致脑动脉炎性增强；而SAL干预可降低SUS大鼠脑动脉中IL-1β染色荧光强度和蛋白表达（均P<0.01）。与CON组相比，急性分离的SUS组脑动脉平滑肌细胞内ROS染色荧光强度显著增加（P<0.01），SOD2染色荧光强度和蛋白表达显著增加（P<0.01）；而SAL干预可降低急性分离的SUS大鼠脑动脉平滑肌细胞内ROS和SOD2染色荧光强度（P均<0.05）以及降低SOD2蛋白表达（P<0.01）。
结论 SAL可减轻模拟失重大鼠脑动脉中的炎性反应，其机制可能与抑制线粒体内氧化应激损伤有关。

Abstract:
AIM To investigate whether salidroside can reduce the inflammation of cerebral artery in simulated weightlessness rats by inhibiting mitochondrial oxidative stress.
METHODS Hindlimb unloading tail suspension was performed in rats. Twenty-four male Sprague-Dawley rats were randomly divided into a control group (CON), a control+salidroside group (CON+SAL), a tail suspended group (SUS) and a tail suspended+salidroside group (SUS+SAL). After tail suspension for one week, the fluorescence intensity of interleukin-1β (IL-1β) and mitochondrial SOD (SOD2) in cerebral arteries were detected by immunofluorescence assay, the changes of interleukin-1β (IL-1β) mRNA levels in cerebral arteries were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and the protein expressions of IL-1β and SOD2 of cerebral artery were detected by Western Blot. The ROS content in mitochondria of acutely isolated cerebral artery smooth muscle cells stained by MitoSox was observed under confocal microscope.
RESULTS Compared with those in CON group, the fluorescence intensity and protein expression of IL-1β of the cerebral artery in SUS group were significantly increased (both, P<0.01) and the mRNA level was increased (P<0.05), suggesting that SUS could enhance cerebral arteritis inflammation. However, salidroside decreased the fluorescence intensity and protein expression of IL-1β staining in SUS rats (both, P<0.01). Compared with those in CON group, the fluorescence intensity of ROS staining in the acutely isolated SUS group was significantly increased (P<0.01), and SOD2 fluorescence intensity and protein expression were significantly increased (P<0.01). However, salidroside reduced the fluorescence intensity of ROS and SOD2 staining in the acutely isolated SUS rat cerebral artery smooth muscle cells (P<0.05) and decreased SOD2 protein expression (P<0.01).
CONCLUSION Salidroside reduces the inflammatory response in the cerebral arteries of simulated hypocritical rats and the mechanism may be related to the inhibition of oxidative stress damage in mitochondria.

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