ArticleExperimental physiology2026
Neuroprotective effects of sinomenine and metformin in diabetic stroke: Role of NLRP3/caspase-1 and mitophagy.
Article in Experimental physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Neuroprotective effects and mechanistic insights of sinomenine in ischemic stroke: a systematic review and meta-analysis of preclinical animal studies.Frontiers in pharmacology · 2026Pooled it
- Polydatin Inhibits Neuroinflammation in Cerebral Ischemia-Reperfusion Injury Through Suppressing the CXCL3/CXCR2 Axis.CNS neuroscience & therapeutics · 2026Article
- Neuroprotective effects of sinomenine and metformin in diabetic stroke: Role of NLRP3/caspase-1 and mitophagy.Experimental physiology · 2026Article
- Metformin Beyond Glycemic Control: Cardiovascular Protection and Diabetes Prevention.Journal of cardiovascular development and disease · 2026Review
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3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes mellitus (T2DM) significantly increases the risk and severity of cerebral ischaemia-reperfusion (IR) injury, yet effective neuroprotective treatments for diabetic stroke remain limited. This study explored whether a combination of sinomenine and metformin could offer enhanced neuroprotection in diabetic rats subjected to cerebral IR injury, and investigated the molecular pathways involved. Male rats were rendered diabetic using a high-fat diet and low-dose streptozotocin. After establishing diabetes, rats underwent transient middle cerebral artery occlusion followed by 24 h of reperfusion. Animals received sinomenine, metformin, or their combination for 7 days prior to IR induction. Neurological function was assessed using standardized behavioural tests. Molecular analyses measured markers of pyroptosis (NLRP3, cleaved caspase-1, gasdermin D N-terminal fragment), mitophagy (PTEN-induced kinase 1 (PINK-1), Parkin), inflammation (interleukin (IL)-1β, IL-18) and oxidative stress (malondialdehyde, superoxide dismutase, glutathione peroxidase). To determine the role of mitophagy, a subset of animals was pretreated with the mitophagy inhibitor mitochondrial division inhibitor 1 (Mdv-1). Combination therapy led to significant improvements in neurological performance, accompanied by downregulation of pyroptosis-associated proteins and pro-inflammatory cytokines, as well as enhanced activation of the PINK-1/Parkin mitophagy pathway and improved antioxidant status. The neuroprotective effects of the combined treatment were abolished by Mdv-1, indicating a critical role for mitophagy in mediating these benefits. The combination of sinomenine and metformin confers additive neuroprotection against cerebral IR injury in diabetic rats, primarily through inhibition of NLRP3-mediated pyroptosis and activation of the PINK-1/Parkin mitophagy pathway. These findings highlight a promising therapeutic strategy for diabetic stroke and warrant further preclinical and clinical investigation.
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