Bacterial Lipopolysaccharide Vigorously Activate JAK2/STAT3 Induced Rheumatoid Arthritis Collate with Complete Freund's Adjuvant in Experimental Rats
Omnia Ahmed Mohamed Abd El-Gaphar1
, Amira Mourad Abo-youssef2 and Gouda Kamel Helal31Pharmacology and Toxicology Department, Faculty of Pharmacy, Nahda University, Egypt.
2Pharmacology and Toxicology Department, Faculty of Pharmacy, Beni-Sueif University, Egypt.
3Pharmacology and Toxicology Department, Faculty of Pharmacy, Al-Azhar University, Egypt.
Corresponding Author E-mail: Omneaahmed25@yahoo.com
Abstract: The Janus kinase-signal transducers and activators of transcription (JAK/STAT) is one of signaling pathways that mediate rheumatoid arthritis (RA) pathogenesis. Present study designed to evaluate the stimulatory role of lipopolysaccharide (LPS) JAK2/STAT3-induced RA, compared to the traditional Complete Freund's Adjuvant (CFA)-induced RA. Rats were allocated into normal control group (saline only), CFA arthritic control groups (0.4 ml/3days/12days, S.C.), and LPS group (100µg/kg/day/12days, I.P.). After 12 days of induction, tissue samples were collected for assessment of tissue phosphorylated JAK2 and STAT3, while serum samples used for biochemical evaluation of interleukin-6 (IL-6) and anti-citrullinated protein antibody (ACPA). Results indicated that LPS significantly increased tissue phosphorylation of JAK2 and STAT3 in cope with significant increase in serum IL-6 and ACPA as compared to CFA. Conclusively, LPS can consider as a formidable inducer for RA, in partly through activation of JAK2/STAT3 signaling pathway, this may add a new approach for experimental induction of RA.
Keywords: Rheumatoid Arthritis; Lipopolysaccaride; JAK2; STAT3 Back to TOC