ArticleInternational journal of molecular sciences2015
Sinomenine hydrochloride protects against polymicrobial sepsis via autophagy.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- The Beneficial Effects of Probiotics via Autophagy: A Systematic Review.BioMed research international · 2021Pooled it
- Cell death signaling and immune regulation: new perspectives on targeted therapy for sepsis.Cellular & molecular biology letters · 2025Review
- Bioactivities and Mechanisms of Action of Sinomenine and Its Derivatives: A Comprehensive Review.Molecules (Basel, Switzerland) · 2024Review
- Emodin protects against intestinal dysfunction and enhances survival in rat model of septic peritonitis through anti-inflammatory actions.Immunity, inflammation and disease · 2023Article
- Current insight on the mechanisms of programmed cell death in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2023Review
- Network pharmacology-based approach to explore the underlying mechanism of sinomenine on sepsis-induced myocardial injury in rats.Frontiers in pharmacology · 2023Article
- Cardiomyocyte death in sepsis: Mechanisms and regulation (Review).Molecular medicine reports · 2022Review
- Sinomenine regulates immune cell subsets: Potential neuro-immune intervene for precise treatment of chronic pain.Frontiers in cell and developmental biology · 2022Review
- Intra-Articular Drug Delivery for Osteoarthritis Treatment.Pharmaceutics · 2021Review
- Sinomenine activation of Nrf2 signaling prevents inflammation and cerebral injury in a mouse model of ischemic stroke.Experimental and therapeutic medicine · 2021Article
- Xinmailong Attenuates Doxorubicin-Induced Lysosomal Dysfunction and Oxidative Stress in H9c2 Cells via HO-1.Oxidative medicine and cellular longevity · 2021Article
- Anti-inflammation Effects of Sinomenine on Macrophages through Suppressing Activated TLR4/NF-κB Signaling Pathway.Current medical science · 2020Article
- Interplay Between NLRP3 Inflammasome and Autophagy.Frontiers in immunology · 2020Review
- Activation of Alpha-7 Nicotinic Acetylcholine Receptors (α7nAchR) Promotes the Protective Autophagy in LPS-Induced Acute Lung Injury (ALI) In Vitro and In Vivo.Inflammation · 2019Article
- Article
- HIPK1 Interference Attenuates Inflammation and Oxidative Stress of Acute Lung Injury via Autophagy.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Circulating extracellular vesicle content revealsJournal of extracellular vesicles · 2019Article
- The Role of Autophagy in Sepsis: Protection and Injury to Organs.Frontiers in physiology · 2019Review
- TRIM28 activates autophagy and promotes cell proliferation in glioblastoma.OncoTargets and therapy · 2019Article
- Overexpression of homeodomain-interacting protein kinase 2 (HIPK2) attenuates sepsis-mediated liver injury by restoring autophagy.Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis, a systemic inflammatory response to infection, is the major cause of death in intensive care units (ICUs). The mortality rate of sepsis remains high even though the treatment and understanding of sepsis both continue to improve. Sinomenine (SIN) is a natural alkaloid extracted from Chinese medicinal plant Sinomenium acutum, and its hydrochloride salt (Sinomenine hydrochloride, SIN-HCl) is widely used to treat rheumatoid arthritis (RA). However, its role in sepsis remains unclear. In the present study, we investigated the role of SIN-HCl in sepsis induced by cecal ligation and puncture (CLP) in BALB/c mice and the corresponding mechanism. SIN-HCl treatment improved the survival of BALB/c mice that were subjected to CLP and reduced multiple organ dysfunction and the release of systemic inflammatory mediators. Autophagy activities were examined using Western blotting. The results showed that CLP-induced autophagy was elevated, and SIN-HCl treatment further strengthened the autophagy activity. Autophagy blocker 3-methyladenine (3-MA) was used to investigate the mechanism of SIN-HCl in vitro. Autophagy activities were determined by examining the autophagosome formation, which was shown as microtubule-associated protein light chain 3 (LC3) puncta with green immunofluorescence. SIN-HCl reduced lipopolysaccharide (LPS)-induced inflammatory cytokine release and increased autophagy in peritoneal macrophages (PM). 3-MA significantly decreased autophagosome formation induced by LPS and SIN-HCl. The decrease of inflammatory cytokines caused by SIN-HCl was partially aggravated by 3-MA treatment. Taken together, our results indicated that SIN-HCl could improve survival, reduce organ damage, and attenuate the release of inflammatory cytokines induced by CLP, at least in part through regulating autophagy activities.
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