ArticleActa cirurgica brasileira2025
Hepatoprotective effect of lotus leaf against non-alcoholic fatty liver disease in rats via alteration of AMPK/SIRT1 and Nrf2/HO-1 signaling pathway.
Article in Acta cirurgica brasileira, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Preclinical evaluation of puerarin for the treatment of non-alcoholic fatty liver disease: a systematic review and meta-analysis.Frontiers in pharmacology · 2026Pooled it
- Chemical Composition and Bioactivity ofCurrent issues in molecular biology · 2025Article
- Green-Synthesized Silver Nanoparticles from Garlic Peel Target NF-κB and Redox Imbalance: A Novel Therapeutic Strategy Against Pyrogallol-Induced Hepatotoxicity in Rats.Nanomaterials (Basel, Switzerland) · 2025Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
purposeIn this study, we scrutinized the protective effect of lotus leaf (LF) against high-fat diet (HFD) induced liver injury in rats.
methodsThe rats received the HFD for the induction of non-alcoholic fatty liver disease. Rats received the oral administration of LF (25, 50, and 100 mg/kg, b.w.). The insulin level, organ index, glucose level, hepatic, oxidative stress, lipid and cytokines parameters were measured. The different mRNA expression and histopathology were performed in the hepatic tissue.
resultsLF treatment suppressed the insulin, glucose and HOMA-IR along with organ index (liver index and spleen index). LF treatment altered the level of liver parameters (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transferase) and oxidative stress parameters in the serum, as well as the liver tissue. LF treatment altered the level of lipid parameters and fat parameters (total fat, perirenal fat, abdominal fat, epididymal fat); cytokines (tumor necrosis factor-α, interleukin-1β, interleukin-6, interleukin-10, interleukin-17, interleukin-33); HO-1, and Nrf2. LF treatment altered the mRNA expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, interleukin-10, caspase-3, caspase-9, cytochrome C, cytochrome D, AMP-activated protein kinase (AMPK), sirtuin 1 (SIRT1), FRX-1, liver X Receptor alpha, fibronectin, matrix metalloproteinase-9, inducible nitric oxide synthase, and transforming growth factor-β 1 (TGF-β1). LF treatment suppressed the necrosis of hepatocytes with less inflammatory cell infiltration in the liver tissue along with alteration of liver injury score.
conclusionThe result showed the protective effect of LF against non-alcoholic fatty liver disease via activating the AMPK/SIRT1 and Nrf2/HO-1 pathway activation.
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