ArticleBMC pharmacology & toxicology2021
Saroglitazar improved hepatic steatosis and fibrosis by modulating inflammatory cytokines and adiponectin in an animal model of non-alcoholic steatohepatitis.
Article in BMC pharmacology & toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- Effects of PPARα, PPARγ, and dual PPARα/γ agonists on liver tissue and biochemical markers in NAFLD-induced Wistar rats.Research in pharmaceutical sciences · 2026Article
- Saroglitazar Mitigated Cyclophosphamide-Induced Testicular Injury: Crosstalk Between Oxidative Stress, Inflammation and Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
- Cardioprotective Effects of SAR Through Attenuating Cardiac-Specific Markers, Inflammatory Markers, Oxidative Stress, and Anxiety in Rats Challenged with 5-Fluorouracil.Journal of xenobiotics · 2025Article
- Bilirubin, a hepatoprotective agent that activates SIRT1, PGC-1α, and PPAR-α, while inhibiting NF-κB in rats with metabolic-associated fatty liver disease.Scientific reports · 2024Article
- Alleviation of pulmonary fibrosis by the dual PPAR agonist saroglitazar and breast milk mesenchymal stem cells via modulating TGFß/SMAD pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Altered Mitochondrial Function in MASLD: Key Features and Promising Therapeutic Approaches.Antioxidants (Basel, Switzerland) · 2024Review
- Comparison of the anti-inflammatory and antilipidemic activity of diosmin and saroglitazar in a model of nonalcoholic fatty liver induced by a high-fat diet in Wistar rats.Iranian journal of basic medical sciences · 2024Article
- Curcumin and saroglitazar attenuate diet-induced nonalcoholic steatohepatitis by activating the Nrf2 pathway and suppressing ERK1/2 signaling.Iranian journal of basic medical sciences · 2024Article
- Suppression of TGF-β/Smad3 signaling pathway byIranian journal of basic medical sciences · 2024Article
- An Overview of the Role of Peroxisome Proliferator-activated Receptors in Liver Diseases.Journal of clinical and translational hepatology · 2023Review
- Tumor Necrosis Factor-Alpha and Adiponectin in Nonalcoholic Fatty Liver Disease-Associated Hepatocellular Carcinoma.Cancers · 2023Review
- Review
- Current Therapeutical Approaches Targeting Lipid Metabolism in NAFLD.International journal of molecular sciences · 2023Review
- The ameliorating effect of withaferin A on high-fat diet-induced non-alcoholic fatty liver disease by acting as an LXR/FXR dual receptor activator.Frontiers in pharmacology · 2023Article
- Molecular mechanisms of metabolic associated fatty liver disease (MAFLD): functional analysis of lipid metabolism pathways.Clinical science (London, England : 1979) · 2022Review
- Peroxisome proliferator-activator receptor γ and psoriasis, molecular and cellular biochemistry.Molecular and cellular biochemistry · 2022Review
- Advancements in the treatment of non-alcoholic fatty liver disease (NAFLD).Frontiers in endocrinology · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) have become significant global health concerns. In the present study, we aimed to investigate the effects of saroglitazar, a dual PPARα/γ agonist, fenofibrate, a PPAR-α agonist, and pioglitazone, a PPAR-γ agonist on an animal model of NASH.
methodsMale Wistar rats were fed a high-fat (HF) emulsion via gavage for 7 weeks to induce NASH. The HF-treated rats were grouped into four groups to receive saroglitazar, pioglitazone, fenofibrate, or vehicle. We measured body and liver weight, liver enzymes, serum levels of adiponectin and leptin. We also performed histopathological examinations and gene expression analysis of interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF- α), transforming growth factor-beta (TGF-β), and monocyte chemoattractant protein 1 (MCP-1).
resultsBody weight was markedly normalized by both saroglitazar and fenofibrate, while the liver index only decreased significantly with saroglitazar. Saroglitazar corrected ALT, AST, leptin, and adiponectin levels better than pioglitazone and fenofibrate. All PPAR agonists significantly attenuated the upregulation of the proinflammatory and TGF-β genes, which correlated with the improved steatosis, inflammation of liver tissue, and fibrotic lesions.
conclusionsAs documented by our results, the dual activation of PPARα/γ by saroglitazar could effectively improve steatosis, fibrosis, and aspects of necro-inflammation in the HF-induced NASH model more than fenofibrate and pioglitazone, and it can be more beneficial in the management of NASH.
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