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Strobilanthes barbatus ameliorates adjuvant-induced arthritis in rats through inhibiting TNF-? signaling pathways

  • Unique Paper ID: 152493
  • Volume: 8
  • Issue: 3
  • PageNo: 578-583
  • Abstract:
  • Strobilanthes barbatus belongs to the family Acanthaceae, is an indigenous plant. The plants of this family possess various pharmacological activities such as anti-inflammatory, antioxidant, anti-osteoarthritis, neurological disorder, anti-diabetic and anti-microbial. The plant has not been investigated for its anti-inflammatory and antiarthritic activity. The present study was undertaken to explore its possible anti-inflammatory and antiarthritic activity. Anti-inflammatory activity of alcoholic and aqueous extracts of the leaves was assessed by in vivo methods. This study was evaluated to show that the S.barbatus leaves extracts possess anti-inflammatory activity and have pronounced effects on adjuvant arthritis. Adjuvant (CFA)-induced arthritis (AIA) was developed and used to test the efficacy of S.barbatus on arthritis rats. Rats were given an oral dose of (75mg/kg, 150mg/kg and 300mg/kg,) once daily from days 14 to 28 after the administration of CFA. The pro-inflammatory cytokine levels TNF alpha level in serum were detected by ELISA and Biochemical markers were also estimated for the S.barbatus. X- Ray and HE staining was used to determine representative histological changes in joint tissues. S.barbatus suppressed the release of tumor necrosis factor-alpha. In addition, S.barbatus could also dramatically ameliorate the pathological changes observed in rat joints. Based on the results, we also observed the changes in biochemical expression by reduction of inflammation. These results proved that treatment with S.barbatus is significantly effective for arthritis and inhibiting the TNF alpha signaling pathway may be a potential therapeutic target for treatment of arthritis.
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Cite This Article

  • ISSN: 2349-6002
  • Volume: 8
  • Issue: 3
  • PageNo: 578-583

Strobilanthes barbatus ameliorates adjuvant-induced arthritis in rats through inhibiting TNF-? signaling pathways

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