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Updated: Jan 22, 2026

Induction and Assessment of Ischemia-reperfusion Injury in Langendorff-perfused Rat Hearts
Published on: July 27, 2015
Effects of NLRP6 in Cerebral Ischemia/Reperfusion (I/R) Injury in Rats
Changchang Meng1, Jinyan Zhang2, Luyu Zhang3
1Department of Pathophysiology, Institute of Neuroscience, Chongqing Medical University, Road1, Chongqing, 400016, People's Republic of China.
Abstract:
The NOD-like receptor protein 6 (NLRP6), an intracytoplasmic pattern recognition receptor in the nucleotide-binding domain, leucine-rich repeat-containing (NLR) innate immune receptor family, influences the inflammation reaction. The role of NLRP6 in cerebral ischemia-reperfusion (I/R) injury in rats is unclear. We explore the function of NLRP6 in cerebral I/R injury. The investigators used a middle cerebral artery occlusion/reperfusion model (MCAO) to imitate ischemic injury. We found the peak expression of NLRP6 is in 48-h post-cerebral I/R injury. The expression of NLRP6 siRNA, as well as the expression of protein and mRNA, was detected by Western blot and qRT-PCR. The degree of IL-1β and IL-18 was assessed by ELISA. After downregulating NLRP6, the expression of IL-1β, IL-18, cleaved Caspase-1, and myeloperoxidase (MPO) were reduced. In HE and Nissl staining, pathological injury of brain tissue after downregulating NLRP6 was improved. NLRP6 siRNA decreased the NLRP6-ASC binding states by CO-IP. NRP6 has a pro-inflammatory effect in cerebral I/R injury, which may provide a new target for the treatment of cerebral I/R injury.
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