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  2. The anti-inflammatory effects of Yunnan Baiyao are involved in regulation of the phospholipase A2/arachidonic acid metabolites pathways in acute inflammation rat model

The anti-inflammatory effects of Yunnan Baiyao are involved in regulation of the phospholipase A2/arachidonic acid metabolites pathways in acute inflammation rat model

  • Mol Med Rep. 2017 Oct;16(4):4045-4053. doi: 10.3892/mmr.2017.7104.
Xiaobin Ren 1 Mingzhu Zhang 1 Lingxiang Chen 1 Wanli Zhang 1 Yu Huang 2 Huazhen Luo 3 Ling Li 4 Hongbing He 1
Affiliations

Affiliations

  • 1 Department of Periodontology, The Affiliated Stomatology Hospital of Kunming Medical University, Kunming, Yunnan 650031, P.R. China.
  • 2 Department of Oral Medicine, The First Hospital of Qujing, Qujing, Yunnan 655000, P.R. China.
  • 3 Department of Oral Medicine, The First Hospital of Kunming, Kunming, Yunnan 650011, P.R. China.
  • 4 Biomedical Engineering Research Center, Kunming Medical University, Kunming, Yunnan 650500, P.R. China.
Abstract

The traditional Chinese medicine Yunnan Baiyao (YNB) has been reported to possess anti‑inflammatory properties, however its mechanism of action remains unclear. It was previously reported that YNB ameliorated depression of arachidonic acid (AA) levels in a rat model of collagen-induced arthritis. In the current study, the capacity of YNB to ameliorate inflammation was compared in carrageenan‑induced and AA‑induced acute inflammation of the rat paw with celecoxib and mizolastine, respectively (n=24 per group). The capacity of YNB to affect the Phospholipase A2 (PLA2)/AA pathway (using reverse transcription‑quantitative polymerase chain reaction) and release of inflammatory lipid mediators (by ELISA) were investigated. Celecoxib ameliorated carrageenan‑induced paw edema, and mizolastine ameliorated AA‑induced rat paw edema. YNB alleviated paw edema and inhibited inflammatory cell infiltration in the two models. YNB inhibited production of 5‑LOX AA metabolite leukotriene B4 (LTB4), and suppressed expression of 5‑LOX, cytosolic PLA2 (cPLA2), 5‑LOX‑activating protein, and LTB4 receptor mRNA in the AA‑induced inflammation model (P<0.05). YNB Inhibited the production of the COX‑2 AA metabolite prostaglandin E2 (PGE2) and suppressed expression of COX‑2, cPLA2, PGE2 mRNA in the carrageenan‑induced inflammation mode (P<0.05). Taken together, the data suggest that modulation of COX and LOX pathways in AA metabolism represent a novel anti-inflammatory mechanism of YNB.

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