ArticleJournal of cellular and molecular medicine2020
Oridonin prevents insulin resistance-mediated cognitive disorder through PTEN/Akt pathway and autophagy in minimal hepatic encephalopathy.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Liraglutide Attenuates Multiorgan Oxidative, Astroglial, and Mitochondrial Stress Responses in Thioacetamide-Induced Hepatic Encephalopathy.International journal of molecular sciences · 2026Article
- Oridonin ameliorates ulcerative colitis by regulating the PI3K/AKT/mTOR signaling pathway to activate autophagy.International journal of molecular medicine · 2026Article
- The potential role of hydrogen sulfide-autophagy axis in diseases.Journal of physiology and biochemistry · 2025Review
- Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases.Redox biology · 2024Review
- Lipid-Based Nanoparticles in Delivering Bioactive Compounds for Improving Therapeutic Efficacy.Pharmaceuticals (Basel, Switzerland) · 2024Review
- A Simple Computational Approach to Identify Potential Drugs for Multiple Sclerosis and Cognitive Disorders from Expert Curated Resources.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Oridonin: A Review of Its Pharmacology, Pharmacokinetics and Toxicity.Frontiers in pharmacology · 2021Review
- Oridonin prevents insulin resistance-mediated cognitive disorder through PTEN/Akt pathway and autophagy in minimal hepatic encephalopathy.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
8 authors.
Funding
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Abstract
Minimal hepatic encephalopathy (MHE) was characterized for cognitive dysfunction. Insulin resistance (IR) has been identified to be correlated with the pathogenesis of MHE. Oridonin (Ori) is an active terpenoid, which has been reported to rescue synaptic loss and restore insulin sensitivity. In this study, we found that intraperitoneal injection of Ori rescued IR, reduced the autophagosome formation and synaptic loss and improved cognitive dysfunction in MHE rats. Moreover, in insulin-resistant PC12 cells and N2a cells, we found that Ori blocked IR-induced synaptic deficits via the down-regulation of PTEN, the phosphorylation of Akt and the inhibition of autophagy. Taken together, these results suggested that Ori displays therapeutic efficacy towards memory deficits via improvement of IR in MHE and represents a novel bioactive therapeutic agent for treating MHE.
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