Rosiglitazone attenuates the severity of hyperlipidemic severe acute pancreatitis in rats

Abstract

Peroxisome proliferator-activated receptor-γ (PPAR-γ) ligand regulates adipocyte differentiation and insulin sensitivity, and exerts antihyperlipidemic and anti-inflammatory effects. However, the mechanisms by which PPAR-γ ligands affect hyperlipidemia with severe acute pancreatitis (SAP) have not been fully elucidated. The present study investigated the effects of rosiglitazone, a PPAR-γ ligand, on hyperlipidemia with SAP in a rat model. The hyperlipidemia was induced with a high-fat diet and SAP was induced by the administration of sodium taurocholate (TCA). The hyperlipidemia was shown to aggravate the severity of the sodium taurocholate-induced SAP. However, rosiglitazone demonstrated significant antihyperlipidemic and anti-inflammatory effects in the rats with high-lipid diet-induced hyperlipidemia and SAP.

HIF-1α-PPARγ-mTORC1 signalling pathway mediated autophagy induces inflammatory response of pancreatic cells in rats with hyperlipidemic acute pancreatitis

“…The peroxisome proliferators-activated receptor γ(PPARγ) is mainly expressed in liver and adipose tissues and it plays a role in promoting the differentiation and maturation of adipocytes and regulating the activation of signaling pathways responsible for lipid metabolism and the expression of related genes [21]. It is believed that hyperlipidemia can exacerbate the in ammatory response and pathological injury of AP, the mechanisms of which may be related to the down regulation of PPARγ mRNA expression [ 22,23]. For this reason, treatment with PPARγ agonist can relieve the in ammatory response of pancreatic tissues in HLAP.…”

Saikosaponin a attenuates hyperlipidemic pancreatitis in rats via the PPAR‑γ/NF‑κB signaling pathway

“…A series of studies have demonstrated the importance of PPARs in regulating inflammatory pathways in AP, by closely interacting with transcription factors such as NF-κB (48,49). Moreover, the preservation of PPAR expression by its agonists usually modulates inflammation by suppressing the activity of NF-κB, increasing the expression of Iκ-Bα and thereby inhibiting their nuclear transcriptional activity and signaling pathways (25). Previous studies investigated PPARs in inflammatory diseases and also found that PPAR activation mediates the NF-κB pathway and associated factors such as Iκ-Bα, MyD88 and toll-like receptor (TLR) 4 (50,51).…”

“…Serum lipid levels, including TC and TG, were also measured and met the hyperlipidemic criteria (23). The acute pancreatitis model was then further induced according to the methods described by Niyaz et al (25) and Shi et al (26). After a 12-h fast, the hyperlipidemic rats were anesthetized by the intraperitoneal injection of pentobarbital sodium (30 mg/kg).…”