Xia Hong, Zhang Bingbing, Yang Dan, Zhu Chengyue, Zhang Jiudan, Chen Hongbo, Ma Hongzhen, Hu Shouci, Xu Chao, Shi Chengqian, Lu Keda, Zhang Peipei
Department of Nephrology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Postgraduate of Internal Medicine of Traditional Chinese Medicine, Zhejiang Chinese Medical University, Hangzhou, China.
Front Pharmacol. 2021 Apr 27;12:624303. doi: 10.3389/fphar.2021.624303. eCollection 2021.
The Yi-Qi-Jian-Pi-Xiao-Yu-Xie-Zhuo (YQJPXYXZ) formula has been used for treating chronic kidney disease (CKD) for many years with good efficiency based on the cumulative empirical experience of previous practitioners. Impairment of the IGF-1/PI3K/Akt signaling pathway plays an important role in mediating muscle wasting. This study aimed to observe effects of the YQJPXYXZ formula on muscle atrophy in CKD rats and investigate its possible mechanism on regulation of the IGF-1/PI3K/Akt signaling pathway. The 5/6 nephrectomized rats were randomly allocated into 3 groups: the CKD group, the KT (compound α-ketoacid tablets) group, and the YQJPXYXZ group. Besides, sham-operated rats were included as the sham group. All rats were treated for 12 weeks. Results showed that administration of the YQJPXYXZ formula prevented body weight loss and muscle fiber size decrease. Moreover, the YQJPXYXZ formula increased the IGF-1 level of serum and skeletal muscle in CKD rats and enhanced the phosphorylation level of Akt. Furthermore, the YQJPXYXZ formula decreased the Atrogin1 and MuRF1 mRNA and MuRF1 proteins. In conclusion, our data demonstrated that the YQJPXYXZ formula improves muscle wasting in CKD rats, which might be associated with the modulation of the IGF-1/PI3K/Akt signaling pathway and inhibition of the ubiquitin-proteasome system (UPS).
益气健脾消瘀泄浊（YQJPXYXZ）方基于历代医家积累的经验，多年来一直用于治疗慢性肾脏病（CKD），疗效良好。IGF-1/PI3K/Akt信号通路受损在介导肌肉萎缩中起重要作用。本研究旨在观察YQJPXYXZ方对CKD大鼠肌肉萎缩的影响，并探讨其调节IGF-1/PI3K/Akt信号通路的可能机制。将5/6肾切除大鼠随机分为3组：CKD组、KT（复方α-酮酸片）组和YQJPXYXZ组。此外，将假手术大鼠作为假手术组。所有大鼠均治疗12周。结果显示，给予YQJPXYXZ方可防止体重减轻和肌纤维尺寸减小。此外，YQJPXYXZ方可提高CKD大鼠血清和骨骼肌中IGF-1水平，并增强Akt的磷酸化水平。此外，YQJPXYXZ方可降低Atrogin1和MuRF1 mRNA及MuRF1蛋白水平。总之，我们的数据表明，YQJPXYXZ方可改善CKD大鼠的肌肉萎缩，这可能与调节IGF-1/PI3K/Akt信号通路及抑制泛素-蛋白酶体系统（UPS）有关。
