Triptolide Attenuates Muscular Inflammation and Oxidative Stress in a Delayed-Onset Muscle Soreness Animal Model.
Che-Chia HsuChin-Chuan TsaiPo-Yen KoTing-Hsien KwanMing-Yie LiuPo-Ting WuI-Ming JouPublished in: International journal of environmental research and public health (2022)
Delayed-onset muscle soreness (DOMS) is associated with exercise-induced muscle damage and inflammation, which is mainly caused by prolonged eccentric exercise in humans. Triptolide, an extract from the Chinese herb Tripterygium wilfordii Hook F, has been used for treating autoimmune and inflammatory diseases in clinical practice. However, whether triptolide attenuates acute muscle damage is still unclear. Here, we examined the effect of triptolide on carrageenan-induced DOMS in rats. Rats were injected with 3% of carrageenan into their muscles to induce acute left gastrocnemius muscular damage, and triptolide treatment attenuated carrageenan-induced acute muscular damage without affecting hepatic function. Triptolide can significantly decrease lipid hydroperoxide and nitric oxide (NO) levels, proinflammatory cytokine production, and the activation of nuclear factor (NF)-ĸB, as well as increase a reduced form of glutathione levels in carrageenan-treated rat muscles. At the enzyme levels, triptolide reduced the inducible nitric oxide synthase (iNOS) expression and muscular myeloperoxidase (MPO) activity in carrageenan-treated DOMS rats. In conclusion, we show that triptolide can attenuate muscular damage by inhibiting muscular oxidative stress and inflammation in a carrageenan-induced rat DOMS model.
Keyphrases
- oxidative stress
- diabetic rats
- resistance training
- nitric oxide synthase
- nitric oxide
- nuclear factor
- dna damage
- ischemia reperfusion injury
- induced apoptosis
- skeletal muscle
- drug induced
- body composition
- liver failure
- clinical practice
- high intensity
- poor prognosis
- multiple sclerosis
- heat shock
- high glucose
- respiratory failure
- inflammatory response
- endothelial cells
- fatty acid
- binding protein
- lps induced