ArticleIranian journal of basic medical sciences2022
TLR4-IN-C34 protects against acute kidney injury via modulating TLR4/MyD88/NF-κb axis, MAPK, and apoptosis.
Article in Iranian journal of basic medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Influence and molecular mechanism of cinnamaldehyde against ventricular arrhythmia via the TAK1-p38MAPK-NLRP3 pathway.Heart and vessels · 2025Article
- Decoding NLRP3 Inflammasome Activation in Alzheimer's Disease: A Focus on Receptor Dynamics.Molecular neurobiology · 2025Review
- Nanomedicine for Acute Kidney Injury: Precision Delivery Strategies, Therapeutic Breakthroughs, Challenges, and Future Perspectives.International journal of nanomedicine · 2025Review
- Therapeutic potential ofFrontiers in pharmacology · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Objectives: Acute kidney injury (AKI) is a major component of isoproterenol (ISO) induced cardiorenal syndrome. In this study, we investigated the effect of TLR4-IN-C34 as a toll-like receptor (TLR)-4 inhibitor on ameliorating ISO-induced AKI and the possible molecular underlying pathways. Materials and Methods: The study included 4 groups: control group, ISO group (rats received 100 mg/kg ISO in 2 doses 24 hr apart, SC), ISO+C341 and ISO+C343 groups (rats received 1 or 3 mg/kg TLR4-IN-C34 respectively twice one hour before each ISO injection, IP). Results: Obtained results showed that TLR4-IN-C34 injection prior to ISO decreased serum creatinine level Conclusion: It can be concluded that TLR4-IN-C34 ameliorates ISO-induced AKI through anti-inflammatory anti-apoptotic effects and modulation of TLR4 signaling pathways.
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