Authors

Jing Yang1, Yu Chen1, Yiqiang Pang2, *


Departments

1Department of Biochemistry and Molecule Biology, Basic Medical Sciences and Forensic Medicine School, Baotou, PR China - 2Department of Neurosurgery, The fourth Hospital of Baotou, Baotou, PR China

Abstract

Objective: This article explores the occurrence of mitochondrial autophagy and NOD-like receptor thermal protein domain 3 (NLRP3) inflammatory bodies in cerebral ischemia-reperfusion injury and its correlation with neuroinflammatory responses. 

Methods: Thirty-five SD rats were collected and adaptively fed for 1 week before the experiment. Fifteen rats were randomly selected as the sham operation group. Meanwhile, the remaining 20 rats were established as a model of cerebral ischemia-reperfusion injury. Model rats were divided into a model group, an Mdivi-1 (mitochondrial autophagy inhibitor) group, a RAPA group (mitochondrial autophagy agonist group) and a siRNA NLRP3 (Intraventricular injection of siRNA in rats, downregulated NLRP3 expression) group, with each group comprising 5 rats. Mitochondrial autophagy and the expression level of cysteine-aspartic protease (Caspase-1), interleukin-1β (IL-1β), NLRP3, COXIV, mitochondrial outer membrane transposase 40 (Tom 40) and manganese superoxide dismutase (MnSOD) were analysed. 

Results: Mitochondrial autophagy in the model group was significantly stronger than that observed in the sham operation group (P<0.01). The number of mitochondria, COXIV, Tom 40 and MnSOD in the model group were significantly lower than was found in the sham group. The expressions of Caspase-1 and IL-1β in the Mdivi-1 group were significantly higher than in the model group, while the expressions of Caspase-1 and IL-1β in the RAPA group were significantly lower than in the model group. The expressions of Caspase-1 and IL-1β in the Mdivi-1 group were significantly higher than seen in the model group, while the expressions of Caspase-1 and IL-1β in the RAPA group were significantly lower than in the model group. The expressions of NLRP3, IL-1β and Caspase-1 in the model group were significantly higher than the sham operation group displayed. Lastly, the expression of Caspase-1 and IL-1β in the siRNA NLRP3 group was significantly lower than that seen in the model group. 

Conclusion: After cerebral ischemia and reperfusion, mitochondrial autophagy in local brain tissue increases, which can effectively reduce the neuroinflammatory response and relieve neurological deficits. NLRP3 inflammatory bodies can participate in the inflammatory response resulting from cerebral ischemia-reperfusion injury. Downregulating the expression of NLRP3 can inhibit the inflammatory response and promote neural function recovery.

Keywords

Cerebral ischemia-reperfusion injury, mitochondrial autophagy, NLRP3 inflammatory bodies, neuroinflammatory response.

DOI:

10.19193/0393-6384_2021_2_158