Niclosamide as a Prospective Therapeutic in L-Arginine Induced Acute Pancreatitis in Rats; Concerning Autophagic p62/ NF-kB signaling pathway

Autophagic flux impairment is recently reported as a cardinal factor in acute pancreatitis (AP)pathogenesis. Niclosamide, an anthelmintic drug, has been lately proved to be potent autophagyenhancer. The diminution of the various inflammatory factors unrestrained release via autophagyimprovement may helpful improve prognosis AP. This study spots on investigating thepotential ameliorative effect niclosamide autophagic and its consequent curative outcomeon L-arginine-induced AP rats. Thirty male wistar rats were divided into three groups. first oneis control one, second L-arginine induced group, third group treatedL-arginine Serum lipase, amylase, pancreatic tissue homogenate IL6, IL1β, TNFα, NF-kB,oxidative stress biomarkers; glutathione peroxidase activity, Hydroxy-2’-Deoxy-Guanosine totalantioxidant capacity levels evaluated. Besides, DNA-binding activity nuclear erythroidrelated 2 (Nrf-2) was assessed using extract. Both LC3-II subunit &P62 mRNA quantified PCR technique. Morphometric analysis histopathological changeswas done. obtained data showed that improved evidencedby significantly reduced serum lipase amylase levels, which could related improvement ofautophagy evidenced by decreased p62 expression pancreaticcells, addition anti-inflammatory NF-kB proinflammatorycytokines along with improving antioxidant tissue. As manifestedby elevation Nrf-2- DNA binding normalization oxidative biomarkers levels.These results pave way for potential therapeutic role pancreatitis.