Jian-Pi-Yi-Shen Formula Alleviates Chronic Kidney Disease in Two Rat Models by Modulating QPRT/NAD(+)/SIRT3/Mitochondrial Dynamics Pathway.
Jian-Pi-Yi-Shen Formula Alleviates Chronic Kidney Disease in Two Rat Models by Modulating QPRT/NAD(+)/SIRT3/Mitochondrial Dynamics Pathway.
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DOI：
10.1155/2021/6625345
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Li S
中科院分区：
文献类型：
--
作者：
Liu X;Liu S;Zhang B;Luo D;Huang S;Wang F;Zheng L;Lu J;Chen J;Li S
健脾益肾方是一种传统的中草药汤剂，临床上用于治疗慢性肾脏病已有数十年的历史。然而，其潜在的机制尚未完全阐明。本研究旨在检测健脾养阴方治疗慢性肾脏病的疗效，并探讨其作用机制。分别采用5/6肾切除(5/6 NX)和含腺嘌呤饲料喂养的方法建立CKD大鼠模型。灌胃干预剂量为10.89 g/kg/d。用血肌酐(Scr)和血尿素氮(BUN)评价肾功能。用高碘酸-席夫(PAS)染色和Masson‘s三色染色评价肾组织病理学改变。采用酶联免疫吸附测定试剂盒检测烟酰胺腺嘌呤二核苷酸(NAD+)水平。免疫印迹法检测肾纤维化、喹啉酸磷酸核糖基转移酶(QPRT)、sirtuin 3(SIRT3)和线粒体动力学的蛋白表达。结果表明，健肾养肾冲剂能显著降低CKD大鼠血清Scr和BUN水平，改善肾小管萎缩和间质纤维化，减少肾细胞外基质沉积。此外，CKD大鼠表现为QPRT/NAD+/SIRT3信号受抑制，线粒体分裂增加，线粒体融合减少。JPYSF治疗可促进QPRT/NAD+/SIRT3信号转导，恢复线粒体分裂/融合平衡。综上所述，JPYSF有效地缓解了两种模型大鼠CKD的进展，这可能与调节QPRT/NAD+/SIRT3/线粒体动力学通路有关。
Jian-Pi-Yi-Shen formula (JPYSF) is a traditional Chinese herbal decoction and has been used for treating chronic kidney disease (CKD) in clinics for decades. However, the potential mechanisms have not been fully elucidated. This study was designed to test the efficacy of JPYSF in treating CKD and explore the underlying mechanism. Two CKD rat models were established by 5/6 nephrectomy (5/6 Nx) and feeding with adenine-containing feed, respectively. The intervention dose of JPYSF was 10.89 g/kg/d by gastric irrigation. Renal function was assessed by serum creatinine (Scr) and blood urea nitrogen (BUN). Periodic acid-Schiff (PAS) and Masson's trichrome staining were used to evaluate renal histopathological changes. The levels of nicotinamide adenine dinucleotide (NAD+) were measured by using the enzyme-linked immunosorbent assay kit. The proteins expressions of renal fibrosis, quinolinate phosphoribosyltransferase (QPRT), sirtuin 3 (SIRT3), and mitochondrial dynamics were determined and quantified by Western blot analysis. The results show that administration of JPYSF significantly lowered Scr and BUN levels, improved renal tubular atrophy and interstitial fibrosis, and decreased renal extracellular matrix deposition in two CKD rat models. In addition, CKD rats exhibited suppressed QPRT/NAD+/SIRT3 signal, increased mitochondrial fission, and decreased mitochondrial fusion. JPYSF treatment promoted QPRT/NAD+/SIRT3 signal and restored mitochondrial fission/fusion balance. In conclusion, administration of JPYSF effectively alleviated CKD progression in two rat models, which may be related with regulation of the QPRT/NAD+/SIRT3/mitochondrial dynamics pathway.
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影响因子：
7.4
作者：
Ozden, Ozkan;Park, Seong-Hoon;Wagner, Brett A.;Song, Ha Yong;Zhu, Yueming;Vassilopoulos, Athanassios;Jung, Barbara;Buettner, Garry R.;Gius, David
通讯作者：
Gius, David
非阿里斯洛胆道酸开了中草药和慢性肾脏疾病患者死亡率的风险：基于人群的随访研究的结果。
影响因子：
2.9
作者：
Hsieh CF;Huang SL;Chen CL;Chen WT;Chang HC;Yang CC
通讯作者：
Yang CC
影响因子：
29
作者：
Qiu, Xiaolei;Brown, Katharine;Chen, Danica
通讯作者：
Chen, Danica
影响因子：
4.2
作者：
Klimova, Nina;Long, Aaron;Kristian, Tibor
通讯作者：
Kristian, Tibor
DOI：
10.1155/2017/5632195
发表时间：
2017-01-01
影响因子：
--
作者：
Hsieh, Chuan-Fa;Chang, Huan-Cheng;Yang, Chen-Chang
通讯作者：
Yang, Chen-Chang