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

  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.