1.甘肃中医药大学药学院,兰州 730030
2.甘肃省第二人民医院药学部,兰州 730099
3.甘肃省中医院科研制剂中心,兰州 730050
Received:17 December 2025,
Revised:2026-04-20,
Accepted:21 April 2026,
Published:15 May 2026
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张晴,马新换,杨明静,等.镰形棘豆炮制品改善大鼠肾纤维化的作用及机制研究 [J].中国药房,2026,37(09):1167-1172.
ZHANG Qing,MA Xinhuan,YANG Mingjing,et al.Study on the effect and mechanism of processed Oxytropis falcata in improving renal fibrosis in rats[J].ZHONGGUO YAOFANG,2026,37(09):1167-1172.
张晴,马新换,杨明静,等.镰形棘豆炮制品改善大鼠肾纤维化的作用及机制研究 [J].中国药房,2026,37(09):1167-1172. DOI: 10.6039/j.issn.1001-0408.2026.09.10.
ZHANG Qing,MA Xinhuan,YANG Mingjing,et al.Study on the effect and mechanism of processed Oxytropis falcata in improving renal fibrosis in rats[J].ZHONGGUO YAOFANG,2026,37(09):1167-1172. DOI: 10.6039/j.issn.1001-0408.2026.09.10.
目的
2
研究镰形棘豆炮制品对肾纤维化(RF)大鼠的改善作用及机制。
方法
2
采用腺嘌呤构建RF模型大鼠。造模成功后,将大鼠分为模型组、阳性对照组(秋水仙碱,0.45 mg/kg)及镰形棘豆炮制品低、中、高剂量组(0.5、1、2 g/kg),另设不造模的空白组,每组8只。阳性对照组和镰形棘豆炮制品各剂量组大鼠灌胃相应药液,空白组和模型组大鼠灌胃等体积生理盐水,每天1次,连续28 d。观察大鼠肾脏外观和肾组织病理学形态;检测大鼠血清中肾功能指标[血尿素氮(BUN)、肌酐(Cr)
]
和炎症因子[白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)
]
水平;检测大鼠肾组织中纤连蛋白(FN)、
α
-平滑肌肌动蛋白(
α
-SMA)、Ⅰ型胶原(Col-Ⅰ)表达水平;检测肾组织中转化生长因子β
1
(TGF-β
1
)、Smad3、胞外信号调节激酶1(ERK1)、ERK2 mRNA表达水平以及TGF-β
1
蛋白表达水平和Smad3、ERK1/2蛋白磷酸化水平。
结果
2
与空白组比较,模型组大鼠肾脏体积增大,颜色苍白且表面粗糙不平;肾小管可见大量炎症细胞浸润和空泡化细胞,胶原纤维增生明显;血清中BUN、Cr、IL-6、TNF-α水平,肾组织中
α
-SMA、Col-Ⅰ、FN蛋白和TGF-β
1
、Smad3、ERK1、ERK2 mRNA表达水平以及TGF-β
1
蛋白表达水平和Smad3、ERK1/2蛋白磷酸化水平均显著升高(
P
<0.05)。与模型组比较,镰形棘豆炮制品各剂量组大鼠肾脏病理改变减轻,炎症细胞浸润和胶原纤维增生减少;上述定量指标水平均显著逆转(
P
<0.05)。
结论
2
镰形棘豆炮制品可改善RF大鼠肾功能,减轻炎症反应和胶原纤维异常沉积,其作用机制可能与抑制TGF-β
1
/Smad信号通路活性有关。
OBJECTIVE
2
To investigate the improvement effect and mechanism of processed
Oxytropis falcata
on renal fibrosis (RF) in rats.
METHODS
2
RF model was induced by adenine. After modeling, the rats were divided into the model group, positive control group (colchicine, 0.45 mg/kg), and processed
O. falcata
low-, medium- and high-dose groups (0.5, 1, 2 g/kg), respectively. Additionally, a blank group without modeling was set up, with 8 rats in each group. The positive control group and the various dosage groups of processed
O. falcata
were given the corresponding medicinal solutions intragastrically, while the blank group and model group were given equal volume of normal saline intragastrically, once daily for 28 consecutive days. The appearance and histopathological morphology of the rats’ kidneys were observed. Serum levels of renal function indexes [bl
ood urea nitrogen (BUN), creatinine (Cr)
]
and inflammatory factors [interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)
]
in rats were detected. Protein expressions of fibronectin (FN),
α
-smooth muscle actin (
α
-SMA) and collagen type Ⅰ (Col-Ⅰ) in renal tissue of rats were determined. mRNA expressions of transforming growth factor-β
1
(TGF-β
1
), Smad3 and extracellular signal-regulated kinase 1/2 (ERK1/2) in renal tissues were measured. Protein expression of TGF-β
1
and phosphorylation levels of Smad3 and ERK1/2 in renal tissues were detected.
RESULTS
2
Compared with the blank group, the rats in the model group exhibited enlarged kidneys with pale color, rough and uneven surface. There was a significant infiltration of inflammatory cells and vacuolated cells in the renal tubules, along with marked proliferation of collagen fibers. Serum levels of BUN, Cr, IL-6 and TNF-α, protein expressions of
α
-SMA, Col-Ⅰ and FN in renal tissues, mRNA expressions of TGF-β
1
, Smad3, ERK1 and ERK2 and protein expression of TGF-β
1
as well as phosphorylation levels of Smad3 and ERK1/2 in renal tissues were increased significantly (
P
<0.05). Compared with the model group, renal pathological changes of rats were alleviated in processed
O. falcata
groups, with reduced infiltration of inflammatory cells and proliferation of collagen fibers. The levels of the aforementioned quantitative indicators were all significantly reversed (
P
<0.05).
CONCLUSIONS
2
Processed
O. falcata
can improve renal function in RF rats, alleviate inflammatory responses, and reduce abnormal collagen fiber deposition. Its mechanism of action may be related to the inhibition of the activity of the TGF-β
1
/Smad signaling pathway.
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