Abstract
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).
Highlights
chronic kidney disease (CKD) is characterized by progressive decline in renal function over months or years and is an increasing public health issue (Webster et al, 2017)
In the 5/6 nephrectomy groups, the YQJPXYXZ formula significantly decreased Serum creatinine (Scr) and blood urea nitrogen (BUN) levels, while KT significantly decreased Scr and tended to decrease BUN compared with the CKD group
The YQJPXYXZ formula was found to reduce the levels of Scr and BUN compared with the KT group
Summary
CKD is characterized by progressive decline in renal function over months or years and is an increasing public health issue (Webster et al, 2017). The diagnosis of PEW mainly includes four aspects as follows: Formula Improves Muscle Atrophy biochemical criteria; low body weight, reduced total body fat, or weight loss; a decrease in muscle mass; and low protein or energy intakes (Fouque et al, 2008). Many factors result in or accelerate muscle wasting in kidney disease These include inflammation, acidosis (Kalantar-Zadeh et al, 2004), hemodialysis (HD) treatment (Kaplan et al, 1995), hyperglucagonemia (Sherwin et al, 1976), hyperparathyroidism (Kopple et al, 1980), endocrine disorders such as resistance to insulin (Mak, 1996) and insulin-like growth factor-1(IGF-1) (Ding et al, 1996), and so on. The IGF-1/PI3K/Akt pathway promoting muscle hypertrophy prevents expression of muscle atrophy–induced UPS, namely, the muscle-specific ubiquitin ligases Atrogin and MuRF1 (Stitt et al, 2004)
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