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贯众提取物通过抑制氧化应激和炎症反应改善乙二醇诱导的大鼠尿石症。

Pyrrosia petiolosa Extract Ameliorates Ethylene Glycol-Induced Urolithiasis in Rats by Inhibiting Oxidative Stress and Inflammatory Response.

机构信息

Department of Pharmacy, The People's Hospital of Shouguang, Shouguang, Shandong 262700, China.

Department of Urology, The People's Hospital of Shouguang, Shouguang, Shandong 262700, China.

出版信息

Dis Markers. 2022 Aug 5;2022:1913067. doi: 10.1155/2022/1913067. eCollection 2022.

DOI:10.1155/2022/1913067
PMID:35968503
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9374559/
Abstract

OBJECTIVE

To study the therapeutic effect and mechanism of Pyrrosia petiolosa (P. petiolosa) extract on ethylene glycol- (EG-) induced urolithiasis in rats.

METHODS

Thirty SD male rats were randomly divided into five groups ( = 6): control group, EG group, and P. petiolosa group (25 mg/kg, 50 mg/kg group, and 100 mg/kg). Biochemical testing was adopted for measuring the blood and urine parameters, as well as the level of superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde acid (MDA) in kidney tissues. HE staining and ELISA were utilized to observe the histopathological changes and detect the level of IL-1, IL-6, MCP-1, and TNF- in the kidney tissue, respectively. And western blot was performed for checking NOX2, NOX4, TGF-1, p-Smad3, Smad3, p-Smad2, and Smad2 protein expression level in kidney tissues.

RESULTS

EG could significantly increase the level of blood urea nitrogen, creatinine, and Na in serum and 24-hour urinary protein, oxalate, uric acid, creatinine, calcium, and phosphorus in urine and decreased the urine volume in rats. Whereas P. petiolosa extract was able to greatly decrease the level of related parameters in serum and urine in a dose-dependent manner, but did not affect the urine pH. In addition, P. petiolosa extract notably ameliorated EG-induced renal tissue injury. Compared with the EG group, P. petiolosa extract markedly raised the level of SOD and GSH and decreased the MDA level and the expression of NOX2 and NOX4 in the kidney tissue. Moreover, P. petiolosa extract also lowered the level of IL-1, IL-6, MCP-1, and TNF- in EG-stimulated kidney tissue and inhibited the protein level of EG-induced TGF-1, p-Smad3, and p-Smad2 in a concentration-dependent manner.

CONCLUSION

P. petiolosa extract can improve EG-induced urolithiasis in rats by inhibiting oxidative stress, inflammatory response, and the activation of TGF- pathway.

摘要

目的

研究贯众(Pyrrosia petiolosa)提取物对乙二醇(EG)诱导的大鼠尿石症的治疗作用及其机制。

方法

30 只 SD 雄性大鼠随机分为 5 组(每组 6 只):对照组、EG 组和贯众组(25、50 和 100mg/kg)。采用生化检测法测定血、尿参数以及肾组织中超氧化物歧化酶(SOD)、谷胱甘肽(GSH)和丙二醛(MDA)的水平。采用 HE 染色和 ELISA 分别观察肾组织的组织病理学变化和检测肾组织中白细胞介素-1(IL-1)、白细胞介素-6(IL-6)、单核细胞趋化蛋白-1(MCP-1)和肿瘤坏死因子-α(TNF-α)的水平。Western blot 检测肾组织中 NADPH 氧化酶 2(NOX2)、NOX4、转化生长因子-β1(TGF-β1)、磷酸化 Smad3、Smad3、磷酸化 Smad2 和 Smad2 蛋白的表达水平。

结果

EG 可显著增加大鼠血清中血尿素氮、肌酐和 Na+水平及 24 小时尿蛋白、草酸、尿酸、肌酐、钙和磷含量,减少尿量,而贯众提取物可显著降低各剂量组血清和尿液中相关参数水平,且呈剂量依赖性,但对尿液 pH 无影响。此外,贯众提取物可明显改善 EG 诱导的肾组织损伤,与 EG 组相比,贯众提取物可显著提高肾组织中 SOD 和 GSH 水平,降低 MDA 水平及 NOX2 和 NOX4 的表达,还可降低 EG 刺激肾组织中 IL-1、IL-6、MCP-1 和 TNF-α 的水平,并呈浓度依赖性抑制 EG 诱导的 TGF-β1、磷酸化 Smad3 和磷酸化 Smad2 蛋白的表达。

结论

贯众提取物可通过抑制氧化应激、炎症反应和 TGF-β 通路的激活,改善 EG 诱导的大鼠尿石症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/77f3fae54e29/DM2022-1913067.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/841a3b3e9063/DM2022-1913067.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/317f7cf38d50/DM2022-1913067.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/0637b99f379d/DM2022-1913067.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/93544c7a2189/DM2022-1913067.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/77f3fae54e29/DM2022-1913067.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/841a3b3e9063/DM2022-1913067.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/317f7cf38d50/DM2022-1913067.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/0637b99f379d/DM2022-1913067.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/93544c7a2189/DM2022-1913067.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7ff/9374559/77f3fae54e29/DM2022-1913067.005.jpg

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