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Tetramethylpyrazine attenuates PPAR-γ antagonist-deteriorated oxazolone-induced colitis in mice
Xiangyi He1, Zhong Zheng, Xiangyi Yang
1Department of Gastroenterology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Abstract:
Tetramethylpyrazine (TMP) is suggested to have anti-inflammatory activity. The aim of this study was to determine the role of peroxisome proliferator activated receptor γ (PPAR-γ) signaling in the pharmacologic effect of TMP on oxazolone (OXZ)-induced colitis. TMP (80 mg/kg/day i.p.) was administered daily 48 h after intrarectal instillation of OXZ, with or without PPAR-γ inhibitor [bisphenol A diglycidyl ether (BADGE) 30 mg/kg] during the 4 days before sacrifice. The inflammatory response was assessed by the disease activity index, macroscopy, histology and myeloperoxidase (MPO) activity. Expression levels of PPAR-γ, NF-κB p65, COX-2, iNOS and TNF-α mRNA in colon mucosa were determined by FQ-PCR, levels of PPAR-γ and NF-κB p65 protein were analyzed by immunohistochemistry, and the total and phosphorylated levels of p38 MAPK were assessed by western blotting. TMP significantly attenuated the damage caused by OXZ and substantially reduced the rise in MPO activity, TNF-α, iNOS, NF-κB p65 and COX-2 expression, as well as the increase in PPAR-γ production; however, no changes in the activation of p38 MAPK were observed. Inhibition of PPAR-γ signaling aggravated inflammation of colon mucosa, and increased p38 phosphrylation. TMP counteracted the effect of inhibition of PPAR-γ. We suggest that the effect of TMP treatment in ulcerative colitis may be related to PPAR-γ signaling, but is independent of PPAR-γ.
Insights
Tetramethylpyrazine (TMP) reduces inflammation in oxazolone-induced colitis by influencing peroxisome proliferator activated receptor γ (PPAR-γ) signaling. This study suggests TMP
Area of Science:
- Pharmacology
- Gastroenterology
- Inflammation Research
Background:
- Tetramethylpyrazine (TMP) exhibits potential anti-inflammatory properties.
- Oxazolone (OXZ)-induced colitis serves as a model for inflammatory bowel disease.
- Peroxisome proliferator activated receptor γ (PPAR-γ) signaling is implicated in inflammatory processes.
Purpose of the Study:
- To investigate the role of PPAR-γ signaling in the anti-inflammatory effects of TMP on OXZ-induced colitis.
- To elucidate the molecular mechanisms underlying TMP's therapeutic action in colitis.
Main Methods:
- Administration of TMP and a PPAR-γ inhibitor (BADGE) in an OXZ-induced colitis model.
- Assessment of inflammatory markers including disease activity index, MPO activity, and histological damage.
- Quantification of gene and protein expression for PPAR-γ, NF-κB p65, COX-2, iNOS, TNF-α, and p38 MAPK.
Main Results:
- TMP significantly attenuated OXZ-induced colitis damage and reduced inflammatory markers (MPO, TNF-α, iNOS, NF-κB p65, COX-2).
- TMP treatment normalized increased PPAR-γ production but did not affect p38 MAPK activation.
- PPAR-γ inhibition exacerbated colitis and increased p38 phosphorylation, effects counteracted by TMP.
Conclusions:
- TMP exerts anti-inflammatory effects in OXZ-induced colitis, potentially mediated through PPAR-γ signaling.
- The therapeutic action of TMP in ulcerative colitis appears linked to PPAR-γ pathways, independent of p38 MAPK activation.
