title: Modulation of T-helper cytokines and inflammatory mediators by Atropa accuminata. Royle in adjuvant induced arthritic tissues.
abstract: BACKGROUND
  Atropa acuminata has been widely used in traditional medicine against arthritis and several associated inflammatory disorders.
  
  
  OBJECTIVE
  The present study was undertaken to investigate the anti-arthritic activities of ethanolic extract of Atropa accuminata (AAEE) and to explore the probable mechanism of action.
  
  
  METHODS
  The anti-arthritic activity of AAEE was evaluated within a dose range of 125-500 mg/kg b.w. in adjuvant induced-arthritis in male wistar rats. An array of pro-inflammatory mediators (PGE2 NO, IL-1β and LTB4) and T-cell-mediated cytokines (IL-2, TNF-a, IFN-c, IL-4, IL-10, IL-12, IL-17, IL-6) were assayed in arthritic paw tissue homogenate of the treated animals. In addition the effects on arthritic lesions, changes in body weight; haematological (Hb, ESR, WBC and RBC) and biochemical parameters (SOD, GSH, GR) and the serum markers (CRP, RF) were also observed.
  
  
  RESULTS
  Significant anti-arthritic activity was observed for AAEE in the polyarthiritis test both in the developing and developed phase of the disease. This was associated with dose dependant suppression of pro-inflammatory mediators (PGE2, NO, IL-1β and LTB4)., Th1-Th17 cytokines (IL-2, TNF-α, IFN-γ, IL-12, IL-17, IL-6) and upregulation of Th2 cytokines (IL-4 and IL-10). AAEE was also observed to protect rats against the primary and secondary arthritic lesions, body weight changes and haematological perturbations. In addition, inhibitory effects of AAEE on biochemical parameters and the serum markers further confirmed that it reduced signs on chronic inflammatory responses.
  
  
  CONCLUSIONS
  The present investigation therefore suggested that AAEE is a potent anti-arthritic agent. The multipronged attack on the inflammatory mediators and T-helper cytokines and strong potency of AAEE may have relevance for inhibition of the chronic inflammatory responses in arthritis.
authors.affiliation: Department of Biochemistry, University of Kashmir, Srinagar-190006, J&K, India.
authors.forename: Albeena
authors.initials: A
authors.lastname: Nisar
authors.affiliation: Indian Institute of Integrative Medicine, Srinagar, India.
authors.forename: Nayeema
authors.initials: N
authors.lastname: Akhter
authors.affiliation: PK-PD Division, Indian Institute of Integrative Medicine, Jammu, India.
authors.forename: Gurudarshan
authors.initials: G
authors.lastname: Singh
authors.affiliation: Department of Botany, University of Kashmir, Srinagar-190006, J&K, India.
authors.forename: Akbar
authors.initials: A
authors.lastname: Masood
authors.affiliation: Department of Biochemistry, University of Kashmir, Srinagar-190006, J&K, India.
authors.forename: Akhter
authors.initials: A
authors.lastname: Malik
authors.affiliation: Government Medical College, Srinagar, J&K, India.
authors.forename: Basharat
authors.initials: B
authors.lastname: Banday
authors.affiliation: Department of Biochemistry, University of Kashmir, Srinagar-190006, J&K, India. Electronic address: zargarafzal01@gmail.com.
authors.forename: Mohammed Afzal
authors.initials: MA
authors.lastname: Zargar
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000737:chemistry / Q000494:pharmacology; D001169:Arthritis, Experimental / Q000188:drug therapy* / Q000473:pathology; D032282:Atropa / Q000737:chemistry*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004487:Edema / Q000188:drug therapy; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D007249:Inflammation / Q000378:metabolism*; D008297:Male; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D010936:Plant Extracts
keywords: Atropa accuminata; Herbal medicine; IL-10, IL-17, IL-6; IL-1β; IL-4; TNF-α