Glorisa superba Hydroalcoholic Extract from Tubers Attenuates Experimental Arthritis by Downregulating Inflammatory Mediators, and Phosphorylation of ERK/JNK/p-38.
Glorisa superba (GS) is a medicinal plant that has been traditionally used in the treatment of joint pain and rheumatoid arthritis (RA). The present study was carried out to investigate the antiarthritic activity of Glorisa superba hydroalcoholic extract (GSHE) in an adjuvant-induced arthritis (AIA) rat model. Arthritis was induced by sub-plantar administration of complete Freund's adjuvant (CFA) and GSHE (25, 50, or 100 mg/kg/day) was administered orally for 21 consecutive days. Joint diameter was measured on Days 0, 3, 7, 14, and 21. GSHE dose dependently attenuates the increased joint diameter and serum tumor necrosis factor (TNF)-α level following induction of arthritis by adjuvant. This attenuation was well substantiated with reduced mRNA expression of interleukin (IL)-1β, IL-6, TNF-α, and NF-κB. Additionally, GSHE inhibited phosphorylation of the mitogen-activated protein kinases (MAPK) signaling pathway as there was decreased protein expression of MAPK (p-p38/p38 and p-ERK/ERK p-JNK/JNK ratio). Moreover, GSHE in a dose-dependent fashion normalized the redox status of ankle joint (GSH, malonaldialdehyde [MDA], and NO levels and superoxide dismutase [SOD] and catalase [CAT] activities) and displayed decreased inflammatory cell infiltration in histopathological findings. Taken together, these findings indicate that GSHE protects against AIA by modulating MAPK.
a Department of Pharmacology , All India Institute of Medical Sciences (AIIMS) , New Delhi , India.|b Department of Pharmacology , Postgraduate Institute of Medical Education and Research , Chandigarh , India.
Rohit
R
Kumar
a Department of Pharmacology , All India Institute of Medical Sciences (AIIMS) , New Delhi , India.
Yogendra Kumar
YK
Gupta
a Department of Pharmacology , All India Institute of Medical Sciences (AIIMS) , New Delhi , India.
Surender
S
Singh
b Department of Pharmacology , Postgraduate Institute of Medical Education and Research , Chandigarh , India.
Amol
A
Patil
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001169:Arthritis, Experimental / Q000188:drug therapy*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D000070437:Colchicaceae / Q000276:immunology*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D015536:Down-Regulation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007596:Joints / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D048670:MAP Kinase Kinase 4 / Q000378:metabolism; D008297:Male; D023421:Models, Animal; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010936:Plant Extracts / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects
D000893:Anti-Inflammatory Agents; D016207:Cytokines; D018836:Inflammation Mediators; D016328:NF-kappa B; D010936:Plant Extracts; D048049:Extracellular Signal-Regulated MAP Kinases; D048670:MAP Kinase Kinase 4
Adjuvant-induced arthritis; Glorisa superba; oxidative stress; pro-inflammatory cytokines