Umbelliferone β-D-galactopyranoside exerts an anti-inflammatory effect by attenuating COX-1 and COX-2

被引:37
|
作者
Kumar, Vikas [1 ]
Al-Abbasi, F. A. [2 ]
Verma, Amita [1 ]
Mujeeb, Mohd [3 ]
Anwar, Firoz [2 ,4 ]
机构
[1] Sam Higginbottom Inst Agr Technol & Sci, Fac Hlth Sci, Dept Pharmaceut Sci, Allahabad 211007, Uttar Pradesh, India
[2] King Abdulaziz Univ, Fac Sci, Dept Biochem, Jeddah 80200, Saudi Arabia
[3] Jamia Hamdard, Fac Pharm, Dept Pharmacognosy & Phytochem, New Delhi 110062, India
[4] SIP, Dehra Dun, Uttarakhand, India
关键词
INDUCED ARTHRITIS; ANTIFUNGAL ACTIVITY; OXIDATIVE STRESS; ANTIOXIDANT; INHIBITION; LEAVES; RAT; EXTRACTS; MARKER; SYSTEM;
D O I
10.1039/c5tx00095e
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Umbelliferone beta-D-galactopyranoside (UFG) (benzopyrone) is a member of the coumarin family, found in many plants exhibiting numerous pharmacological actions. The current experiments were carried out to exemplify the anti-inflammatory potential of UFG on chronic inflammation induced by Complete Freund Adjuvant (CFA) (heat killed Mycobacterium tuberculosis) in experimental rats. Arthritis in rats was induced by intradermal administration of CFA (0.05 ml) in the right hind paw, and confirmed by development of paw edema and arthritic index in comparison with normal controls. The anti-arthritic activity of UFG was determined by its ability to inhibit various biochemical markers, viz., pro-inflammatory, antioxidant enzymes, and hematological parameters elevated upon administration of CFA. UFG was also tested for its inhibitory activity against cyclooxygenase-1 (COX-1) and COX-2 via enzyme inhibition assay and the results were monitored spectrophotometrically with a 96-well plate reader. The results of the study showed that UFG in a dose of 10, 20 or 40 mg kg(-1) per day, p.o., helps to prevent paw edema and arthritic score development for arthritis in rats. It markedly alters hematological and oxidative stress induced by the adjuvant. Moreover, the changes brought about in inflammation/arthritis serum markers were reverted back to a near normal level upon UFG treatment in a dose dependent manner. Histopathological analysis of the joints of subjects showed UFG significantly decreases mononuclear infiltration and synovial hyperplasia, which confirms the utility of UFG as an anti-arthritic agent. In a COX inhibition assay UFG was found to act prominently to inhibit COX-2 then COX-1, which suggests its plausible mechanism of action. The current study clearly indicates that UFG possesses anti-inflammatory effects against CFA induced arthritis via suppressing COX-2 inhibition.
引用
收藏
页码:1072 / 1084
页数:13
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