[1]苏比奴尔·阿不都克力木,秦旭阳,陆蕾,等.复肾泄浊方通过调节慢性肾脏病大鼠脂肪酸代谢改善肾纤维化机制研究[J].陕西中医,2026,(4):461-466,471.[doi:DOI:10.3969/j.issn.1000-7369.2026.04.005]
 ABUDKELIMU Subinur,QIN Xuyang,LU Lei,et al.Mechanism of Fushen Xiezhuo recipe in ameliorating renal fibrosis in CKD rats by regulating fatty acid metabolism[J].,2026,(4):461-466,471.[doi:DOI:10.3969/j.issn.1000-7369.2026.04.005]
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复肾泄浊方通过调节慢性肾脏病大鼠脂肪酸代谢改善肾纤维化机制研究

《陕西中医》[ISSN:1000-7369/CN:61-1281/TN]

卷:
期数:
2026年4期
页码:
461-466,471
栏目:
基础研究
出版日期:
2026-04-05

文章信息/Info

Title:
Mechanism of Fushen Xiezhuo recipe in ameliorating renal fibrosis in CKD rats by regulating fatty acid metabolism
作者:
苏比奴尔·阿不都克力木1秦旭阳1陆蕾1周蓓2李静茹1舒占钧3
(1.新疆医科大学第四临床医学院,新疆 乌鲁木齐 830000;2.新疆医科大学实验室与设备管理处动物实验中心,新疆 乌鲁木齐 830011;3.新疆医科大学附属中医医院,新疆 乌鲁木齐 830000)
Author(s):
ABUDKELIMU Subinur1QIN Xuyang1LU Lei1ZHOU Bei2LI Jingru1SHU Zhanjun3
(1.The Fourth Clinical Medical College of Xinjiang Medical University,Urumqi 830000,China;2.Animal Experiment Center,Laboratory and Equipment Management Office,Xinjiang Medical University,Urumqi 830000,China;3.The Fourth Affiliated Hospital of Traditional Chinese Medicine of Xinjiang Medical University,Xinjiang Medical University,Urumqi 830000,China)
关键词:
肾纤维化慢性肾脏病脂肪酸代谢复肾泄浊方细胞凋亡线粒体代谢
Keywords:
Renal fibrosisChronic kidney diseaseFatty acid metabolismFushen Xiezhuo formulaApoptosisMitochondrial metabolism
分类号:
R 285
DOI:
DOI:10.3969/j.issn.1000-7369.2026.04.005
文献标志码:
A
摘要:
目的:探讨复肾泄浊方(FSXZF)调节慢性肾脏病(CKD)大鼠脂肪酸代谢改善肾纤维化的机制。方法:将SPF级雄性SD大鼠32只随机分成空白组、模型组和FSXZF低、高剂量组,每组8只。除空白组外,余大鼠予腺嘌呤连续灌胃3周诱导建立CKD大鼠模型,FSXZF低、高剂量组大鼠分别予16.3、32.5 g/(kg·d)FSXZF灌胃4周。观察各组大鼠体重、肾脏指数;测定大鼠肾功能;HE及Masson染色观察肾组织病理改变;油红O染色观察脂质沉积;透射电镜观察线粒体超微结构。Western blot检测肾脏组织Bcl-2相关X蛋白(Bax)、细胞淋巴瘤2(Bcl-2)、半胱氨酸蛋白酶3(Caspase-3)、活化型Caspase-3(C-Caspase-3)的蛋白水平;Real-time PCR检测肾组织过氧化物酶体增殖物激活受体α(PPAR-α)、肉毒碱棕榈酰基转移酶1α(CPT1-α)mRNA水平。结果:与空白组相比,模型组大鼠体重下降,肾重及肾脏指数升高,肾功能指标明显减退(均P<0.05);病理提示大鼠肾小球萎缩、基底膜增厚,肾小管扩张,间质炎症浸润和胶原沉积增加,伴脂质沉积;电镜提示线粒体密度减少、肿胀,嵴断裂减少甚至消失。PPAR-α、CPT1-α mRNA及Bcl-2蛋白表达降低;Bax、Caspase-3、C-Caspase-3、Bax/Bcl-2、C-Caspase-3/Caspase-3蛋白表达上调(均P<0.05)。与模型组比较,FSXZF高剂量组大鼠肌酐、尿素氮、24 h-UTP明显下降(均P<0.05);FSXZF各剂量组肾脏指数降低(均P<0.05),肾脏病理明显改善,脂质沉积减少,线粒体肿胀和嵴损伤缓解;同时上调PPAR-α、CPT1-α mRNA及Bcl-2蛋白表达,下调Bax、C-Caspase-3及相关比值(均P<0.05)。结论:FSXZF可有效缓解腺嘌呤诱导的CKD大鼠肾功能损伤,改善肾脏组织病理及抑制肾纤维化进展,其保护机制可能与调节肾脏脂肪酸代谢,进而抑制肾纤维化有关。
Abstract:
Objective:To investigate Fushen Xiezhuo formula (FSXZF) attenuates adenine-induced renal fibrosis in chronic kidney disease (CKD) rats by modulating renal fatty acid metabolism.Methods:Thirty-two SPF male sprague-dawley rats were randomly assigned to four groups (n=8):control group,model group, low-dose FSXZF (FSXZF-L) group and high-dose FSXZF (FSXZF-H) group.Except for the control group,rats received adenine for 3 consecutive weeks to establish a CKD model,followed by FSXZF administration at 16.3 or 32.5 g/(kg·d) for 4 weeks in the FSXZF-L and FSXZF-H groups,respectively.Body weight and kidney index were recorded.Serum creatinine (SCr),blood urea nitrogen (BUN),uric acid (UA) and 24-h urinary protein were measured.Renal histopathology and collagen volume fraction were evaluated by hematoxylin-eosin (HE) and Masson staining.Lipid deposition was assessed by oil red O staining.And mitochondrial ultrastructure was observed by transmission electron microscopy.Protein expression of Bcl-2-associated X protein (Bax),B-cell lymphoma-2 (Bcl-2),Caspase-3 and Cleaved Caspase-3 in renal tissue was detected by Western blotting.mRNA expression of carnitine palmitoyltransferase-1α (CPT1-α) and peroxisome proliferator-activated receptor α (PPAR-α) was determined by real-time PCR.Results:Compared with the blank group,the body weight of rats in the model group decreased,the kidney weight and kidney index increased,and the renal function indicators significantly declined (all P<0.05).Pathology showed glomerular atrophy,basement membrane thickening,tubular dilation,increased interstitial inflammatory infiltration and collagen deposition,accompanied by lipid deposition in rats.Electron microscopy showed a decrease in mitochondrial density,swelling,and a decrease or even disappearance of broken cristae.The expression of PPAR-α,CPT1-α mRNA and Bcl-2 protein decreased.The expression of Bax,Caspase-3,C-Caspase-3,Bax/Bcl-2,C-Caspase-3/Caspase-3 proteins was up-regulated (all P<0.05).Compared with the model group,the levels of creatinine,blood urea nitrogen and 24 h-UTP in rats of the high-dose FSXZF group decreased significantly (all P<0.05).The kidney index decreased in all FSXZF dose groups (all P<0.05),the renal pathology improved significantly,lipid deposition decreased,and mitochondrial swelling and cristae damage were alleviated.At the same time,the expression of PPAR-α,CPT1-α mRNA and Bcl-2 protein was up-regulated,and the expression of Bax,C-Caspase-3 and related ratios was down-regulated (all P<0.05).Conclusion:FSXZF effectively ameliorates adenine-induced renal dysfunction,improves renal histopathological injury and inhibits the progression of renal fibrosis in CKD rats.Its nephroprotective effects may be associated with modulation of renal fatty acid metabolism,thereby suppressing renal fibrosis.

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备注/Memo

备注/Memo:
新疆维吾尔自治区“天山英才”医药卫生高层次人才项目(TSYC202401A063);新疆维吾尔自治区中医医院中医药传承创新中心临床研究孵化基金资助项目(2025CC02);新疆维吾尔自治区中医医院科研项目(YYZJ2024-002)
更新日期/Last Update: 2026-04-05