Wang Xiaoyue, Xu Yi, Wang Yonghua, Xu Yuyu, Tian Yang, Wang Yanni, Wang Ming
College of Food Science & Engineering, Northwest University, No. 229 Taibai North Road, Xi'an, Shaanxi, 710069, China.
Shaanxi Natural Carbohydrate Resource Engineering Research Center, Northwest University, Xi'an, 710069, China.
Plant Foods Hum Nutr. 2025 Apr 29;80(2):115. doi: 10.1007/s11130-025-01356-1.
The gut microbiota serves a critical role in the development of chronic kidney disease (CKD). High salt intake has been known to cause hypertension and CKD, however, it is still unclear whether it also affects gut microbiota in CKD mice. This article first studied the salutary effects of poricoic acid A (PAA), a natural triterpenoid from Poria cocos, on high salt diet-induced CKD in kunming mice. It was demonstrated that the administration of PAA by oral gavage (20 mg/kg·bw) could decrease the kidney index and urinary protein levels, prevent the kidney tubule dilated and renal fibrosis, and activated the expression of adenosine monophosphate-activated protein kinase (AMPK) in kidney. In addition, 16 S rRNA-based microbiota analysis indicated that PAA ameliorated intestinal microbiota dysbiosis caused by high-salt-diet and particularly enhanced the abundances of beneficial microbiota, such as Lactobacillus and Akkermansia, followed by a significant increase in the levels of short-chain fatty acids (SCFAs). Meanwhile, PAA improved intestinal barrier damage and increased the expression of intestinal tight junction protein. In summary, these experiments demonstrated that PAA enhances the growth of probiotics while decreasing the abundance of endotoxin-producing bacteria. This dual action contributes to the amelioration of intestinal mucosal barrier dysfunction and mitigates the impact of a high-salt diet on renal interstitial fibrosis in mice.
肠道微生物群在慢性肾脏病（CKD）的发展中起着关键作用。已知高盐摄入会导致高血压和CKD，然而，高盐摄入是否也会影响CKD小鼠的肠道微生物群仍不清楚。本文首先研究了茯苓中的天然三萜类化合物茯苓酸A（PAA）对昆明小鼠高盐饮食诱导的CKD的有益作用。结果表明，通过灌胃给予PAA（20mg/kg·bw）可以降低肾脏指数和尿蛋白水平，防止肾小管扩张和肾纤维化，并激活肾脏中腺苷单磷酸激活蛋白激酶（AMPK）的表达。此外，基于16S rRNA的微生物群分析表明，PAA改善了高盐饮食引起的肠道微生物群失调，尤其增加了有益微生物群（如乳酸杆菌和阿克曼氏菌）的丰度，随后短链脂肪酸（SCFAs）水平显著升高。同时，PAA改善了肠道屏障损伤并增加了肠道紧密连接蛋白的表达。总之，这些实验表明，PAA在增加益生菌生长的同时降低了产内毒素细菌的丰度。这种双重作用有助于改善肠道黏膜屏障功能障碍，并减轻高盐饮食对小鼠肾间质纤维化的影响。
