Graduate Institute of Biotechnology, National Chung-Hsing University, Taichung 402, Taiwan.
Department of Veterinary Medicine, National Chung-Hsing University, Taichung 402, Taiwan.
Molecules. 2023 Jan 10;28(2):688. doi: 10.3390/molecules28020688.
Muscle atrophy caused by an imbalance between the synthesis and the degradation of proteins is a syndrome commonly found in the elders. Teaghrelin, a natural compound from oolong tea, has been shown to promote cell differentiation and to inhibit dexamethasone-induced muscle atrophy in C2C12 cells. In this study, the therapeutic effects of teaghrelin on muscle atrophy were evaluated in Sprague Dawley rats treated with dexamethasone. The masses of the soleus, gastrocnemius and extensor digitorum longus muscles were reduced in dexamethasone-treated rats, and the reduction of these muscle masses was significantly attenuated when the rats were supplemented with teaghrelin. Accordingly, the level of serum creatine kinase, a marker enzyme of muscle proteolysis, was elevated in dexamethasone-treated rats, and the elevation was substantially reduced by teaghrelin supplementation. A decrease in Akt phosphorylation causing the activation of the ubiquitin-proteasome system and autophagy for protein degradation was detected in the gastrocnemius muscles of the dexamethasone-treated rats, and this signaling pathway for protein degradation was significantly inhibited by teaghrelin supplementation. Protein synthesis via the mTOR/p70S6K pathway was slowed down in the gastrocnemius muscles of the dexamethasone-treated rats and was significantly rescued after teaghrelin supplementation. Teaghrelin seemed to prevent muscle atrophy by reducing protein degradation and enhancing protein synthesis via Akt phosphorylation.
肌肉萎缩是一种由于蛋白质合成和降解失衡而引起的综合征,常见于老年人。茶红素是一种来自乌龙茶的天然化合物,已被证明可促进细胞分化,并抑制 C2C12 细胞中地塞米松诱导的肌肉萎缩。在这项研究中,评估了茶红素对用地塞米松处理的 Sprague Dawley 大鼠肌肉萎缩的治疗效果。地塞米松处理的大鼠的比目鱼肌、腓肠肌和趾长伸肌的质量减少,而当大鼠补充茶红素时,这些肌肉质量的减少明显减轻。因此,血清肌酸激酶(一种肌肉蛋白水解的标志物酶)的水平在用地塞米松处理的大鼠中升高,而茶红素的补充则大大降低了这种升高。在用地塞米松处理的大鼠的腓肠肌中检测到 Akt 磷酸化减少导致泛素-蛋白酶体系统和自噬的激活,用于蛋白质降解,而这种蛋白质降解的信号通路则明显被茶红素的补充所抑制。通过 mTOR/p70S6K 途径的蛋白质合成在用地塞米松处理的大鼠的腓肠肌中减慢,并且在茶红素补充后显著得到挽救。茶红素似乎通过减少蛋白质降解和通过 Akt 磷酸化增强蛋白质合成来预防肌肉萎缩。