Rosiglitazone attenuates renal injury caused by hyperlipidemic pancreatitis

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Rosiglitazone attenuates renal injury in hyperlipidemic pancreatitis by inhibiting NF-κB and MAPK P38 signaling pathways, thereby relieving inflammation and preventing cell apoptosis.

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Abstract

Hyperlipidemic pancreatitis (HP) is a serious inflammatory disease with very high mortality and multiple organ injuries including renal injury. Rosiglitazone (Ros), an agonist of peroxisome proliferator activated receptor-γ (PPAR-γ), was reported to show a protective role against pancreatitis. However, whether Ros has an effect on renal injury caused by HP is not yet clear. In the present study, the function of Ros was explored using ELISA, RT-PCR, western blot, PAS staining and immunohistochemistry. Results of this study showed that Ros could inhibit the activation of NF-κB and MAPK P38 signaling pathways, relieve inflammatory response and inhibit cell apoptosis, thus attenuating renal injury caused by HP. This study suggested that Ros might be a promising drug for the treatment of renal injury caused by HP and also laid theoretical foundation for the development of renal injury treatment.

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MeSH descriptors

Acute Kidney Injury Acute Kidney Injury Hypoglycemic Agents Pancreatitis Thiazolidinediones Acute Kidney Injury Animals Blotting, Western Disease Models, Animal Enzyme-Linked Immunosorbent Assay Hyperlipidemias Hyperlipidemias Hypoglycemic Agents Immunohistochemistry In Situ Nick-End Labeling Male Pancreatitis Rats Rats, Sprague-Dawley Real-Time Polymerase Chain Reaction

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europepmc
last seen: 2026-10-25T09:32:14.900964+00:00
pubmed
last seen: 2026-10-08T21:15:59.322652+00:00