PDF(Pubmed)
Abstract：
UNASSIGNED: Tubulointerstitial fibrosis (TIF) is a critical pathological feature of chronic renal failure (CRF), with oxidative stress (OS) and hypoxic responses in renal proximal tubular epithelial cells playing pivotal roles in disease progression. This study explores the effects of Modified Zhenwu Tang (MZWT) on these processes, aiming to uncover its potential mechanisms in slowing CRF progression.
UNASSIGNED: We used adenine (Ade) to induce CRF in rats, which were then treated with benazepril hydrochloride (Lotensin) and MZWT for 8 weeks. Assessments included liver and renal function, electrolytes, blood lipids, renal tissue pathology, OS levels, the hypoxia-inducible factor (HIF) pathway, inflammatory markers, and other relevant indicators. In vitro, human renal cortical proximal tubular epithelial cells were subjected to hypoxia and lipopolysaccharide for 72 h, with concurrent treatment using MZWT, FM19G11, and N-acetyl-l-cysteine. Measurements taken included reactive oxygen species (ROS), HIF pathway activity, inflammatory markers, and other relevant indicators.
UNASSIGNED: Ade treatment induced significant disruptions in renal function, blood lipids, electrolytes, and tubulointerstitial architecture, alongside heightened OS, HIF pathway activation, and inflammatory responses in rats. In vivo, MZWT effectively ameliorated proteinuria, renal dysfunction, lipid and electrolyte imbalances, and renal tissue damage; it also suppressed OS, HIF pathway activation, epithelial-mesenchymal transition (EMT) in proximal tubular epithelial cells, and reduced the production of inflammatory cytokines and collagen fibers. In vitro findings demonstrated that MZWT decreased apoptosis, reduced ROS production, curbed OS, HIF pathway activation, and EMT in proximal tubular epithelial cells, and diminished the output of inflammatory cytokines and collagen.
UNASSIGNED: OS and hypoxic responses significantly contribute to TIF development. MZWT mitigates these responses in renal proximal tubular epithelial cells, thereby delaying the progression of CRF.
UNASSIGNED: We used adenine (Ade) to induce CRF in rats, which were then treated with benazepril hydrochloride (Lotensin) and MZWT for 8 weeks. Assessments included liver and renal function, electrolytes, blood lipids, renal tissue pathology, OS levels, the hypoxia-inducible factor (HIF) pathway, inflammatory markers, and other relevant indicators. In vitro, human renal cortical proximal tubular epithelial cells were subjected to hypoxia and lipopolysaccharide for 72 h, with concurrent treatment using MZWT, FM19G11, and N-acetyl-l-cysteine. Measurements taken included reactive oxygen species (ROS), HIF pathway activity, inflammatory markers, and other relevant indicators.
UNASSIGNED: Ade treatment induced significant disruptions in renal function, blood lipids, electrolytes, and tubulointerstitial architecture, alongside heightened OS, HIF pathway activation, and inflammatory responses in rats. In vivo, MZWT effectively ameliorated proteinuria, renal dysfunction, lipid and electrolyte imbalances, and renal tissue damage; it also suppressed OS, HIF pathway activation, epithelial-mesenchymal transition (EMT) in proximal tubular epithelial cells, and reduced the production of inflammatory cytokines and collagen fibers. In vitro findings demonstrated that MZWT decreased apoptosis, reduced ROS production, curbed OS, HIF pathway activation, and EMT in proximal tubular epithelial cells, and diminished the output of inflammatory cytokines and collagen.
UNASSIGNED: OS and hypoxic responses significantly contribute to TIF development. MZWT mitigates these responses in renal proximal tubular epithelial cells, thereby delaying the progression of CRF.
摘要：
■肾小管间质纤维化（TIF）是慢性肾衰竭（CRF）的关键病理特征，肾近端小管上皮细胞的氧化应激（OS）和低氧反应在疾病进展中起关键作用。本研究探讨了改性真武汤(MZWT)对这些过程的影响，旨在揭示其减缓CRF进展的潜在机制。
■我们使用腺嘌呤（Ade）在大鼠中诱导CRF，然后用盐酸贝那普利（Lotensin）和MZWT治疗8周。评估包括肝肾功能，电解质，血脂,肾组织病理学，操作系统级别,缺氧诱导因子（HIF）途径，炎症标志物，等相关指标。体外，人肾皮质近端肾小管上皮细胞经受缺氧和脂多糖72小时，同时使用MZWT治疗，FM19G11和N-乙酰基-1-半胱氨酸。测量包括活性氧（ROS），HIF通路活性,炎症标志物，等相关指标。
■阿德治疗导致肾功能显著中断，血脂,电解质，和肾小管间质结构，与增强的操作系统一起，HIF通路激活,和大鼠的炎症反应。在体内,MZWT有效改善蛋白尿，肾功能不全,脂质和电解质失衡，和肾组织损伤；它还抑制了OS，HIF通路激活,近端肾小管上皮细胞的上皮-间质转化（EMT），并减少炎性细胞因子和胶原纤维的产生。体外研究结果表明，MZWT降低细胞凋亡，减少ROS产生，限制操作系统，HIF通路激活,和近端肾小管上皮细胞的EMT，并减少炎性细胞因子和胶原蛋白的输出。
■OS和低氧反应显著促进TIF的发展。MZWT减轻肾近端小管上皮细胞的这些反应，从而延缓CRF的进展。
■我们使用腺嘌呤（Ade）在大鼠中诱导CRF，然后用盐酸贝那普利（Lotensin）和MZWT治疗8周。评估包括肝肾功能，电解质，血脂,肾组织病理学，操作系统级别,缺氧诱导因子（HIF）途径，炎症标志物，等相关指标。体外，人肾皮质近端肾小管上皮细胞经受缺氧和脂多糖72小时，同时使用MZWT治疗，FM19G11和N-乙酰基-1-半胱氨酸。测量包括活性氧（ROS），HIF通路活性,炎症标志物，等相关指标。
■阿德治疗导致肾功能显著中断，血脂,电解质，和肾小管间质结构，与增强的操作系统一起，HIF通路激活,和大鼠的炎症反应。在体内,MZWT有效改善蛋白尿，肾功能不全,脂质和电解质失衡，和肾组织损伤；它还抑制了OS，HIF通路激活,近端肾小管上皮细胞的上皮-间质转化（EMT），并减少炎性细胞因子和胶原纤维的产生。体外研究结果表明，MZWT降低细胞凋亡，减少ROS产生，限制操作系统，HIF通路激活,和近端肾小管上皮细胞的EMT，并减少炎性细胞因子和胶原蛋白的输出。
■OS和低氧反应显著促进TIF的发展。MZWT减轻肾近端小管上皮细胞的这些反应，从而延缓CRF的进展。
