清肾颗粒通过调控Akt3介导的M1型巨噬细胞极化改善单侧输尿管梗阻小鼠肾纤维化

doi:10.12122/j.issn.1673-4254.2026.06.02

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (6): 1216-1227.doi: 10.12122/j.issn.1673-4254.2026.06.02

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清肾颗粒通过调控Akt3介导的M1型巨噬细胞极化改善单侧输尿管梗阻小鼠肾纤维化

王伟丽(), 高怡琳, 洪馨, 陈义珍, 程梦, 张磊, 戴荣(), 王亿平()

安徽中医药大学第一附属医院肾内科，安徽合肥 230031

收稿日期:2025-12-02 出版日期:2026-06-20 发布日期:2026-06-24
通讯作者: 戴荣,王亿平 E-mail:wang37937379@163.com;azydairong@163.com;wypwyp54@aliyun.com
作者简介:王伟丽，博士，医师，E-mail: wang37937379@163.com
基金资助:
国家自然科学基金(82274307);安徽省自然科学基金项目(2308085MH292);安徽省自然科学基金项目(202407290785);安徽省卫生健康科研项目(AHWJ2024BAc20084);安徽省卫生健康科研项目(AHWJ2024Aa30409);安徽中医药大学临床科研项目(2024YFYLCZX28);合肥市科技局生命健康专项(GJ2022SM03);2023年度合肥综合性国家科学中心大健康研究院新安医学与中医药现代化研究所科研项目(2023CXMMTCM018);国家中医优势专科(国中医药医政函[2024]90号)

Qingshen Granules alleviate renal fibrosis in mice with unilateral ureteral obstruction by regulating Akt3-mediated M1 macrophage polarization

Weili WANG(), Yilin GAO, Xin HONG, Yizhen CHEN, Meng CHENG, Lei ZHANG, Rong DAI(), Yiping WANG()

Department of Nephrology, First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei 230031, China

Received:2025-12-02 Online:2026-06-20 Published:2026-06-24
Contact: Rong DAI, Yiping WANG E-mail:wang37937379@163.com;azydairong@163.com;wypwyp54@aliyun.com
Supported by:
National Natural Science Foundation of China(82274307)

摘要/Abstract

摘要：

目的探究清肾颗粒抑制肾纤维化的作用机制，明确其是否通过调控 Akt3 介导的巨噬细胞极化发挥效应。方法体内构建单侧输尿管梗阻（UUO）小鼠肾纤维化模型，分为假手术组、模型组、清肾颗粒治疗组［4.0 g·kg^-1·d^-1）］，6只/组，灌胃2周；通过 AAV9 介导肾脏Akt3 敲低，设置 Sham+NC、Sham+shAkt3、Model+NC、Model+shAkt3组；体外以TGF-β1 诱导 HK-2细胞纤维化，用清肾颗粒含药血清干预，同时构建HK-2细胞与THP-1来源巨噬细胞的共培养体系。采用 HE、Masson 染色观察肾脏病理变化；ELISA 检测血清肌酐（Scr）、尿素氮（BUN）；Western blotting、RT-qPCR检测Akt3、α-SMA、E-cad、IL-6、TNF-α蛋白及 mRNA 表达；免疫组化、免疫荧光验证蛋白定位；流式细胞术检测巨噬细胞极化表型；CCK-8、EdU 实验评估细胞活力与增殖能力。结果体内实验表明，与假手术组相比，模型组小鼠肾功能显著受损，Scr、BUN水平升高（P<0.05），伴肾小管损伤、肾间质胶原纤维沉积，肾组织IL-6、TNF-α的mRNA及α-SMA蛋白表达上调， E-cad蛋白表达下调（P<0.05）；与模型组相比，清肾颗粒治疗组上述指标均改善（P<0.05）。AAV9介导肾脏特异性Akt3敲低实验中，与Sham+NC组相比，Model+NC组小鼠肾纤维化加重，肾组织M1型巨噬细胞占比升高（P<0.05），M2型无显著变化（P>0.05）；与Model+NC组相比，Model+ shAkt3敲低组肾纤维化减轻，M1型巨噬细胞极化受抑制（P<0.05），M2型仍无明显差异（P>0.05）；清肾颗粒显著下调肾组织 Akt3 蛋白表达，降低 M1 型巨噬细胞比例（P<0.05）。体外实验中，与对照组相比，模型组细胞活力、增殖能力下降，Akt3、α-SMA蛋白上调，E-cad蛋白下调，清肾颗粒含药血清组可逆转上述变化（P<0.05）；流式细胞术检测显示，TGF-β1诱导的HK-2细胞可促进M0巨噬细胞向M1型极化，清肾颗粒含药血清干预后M1型极化被抑制（P<0.05）。结论清肾颗粒通过抑制Akt3介导的M1型巨噬细胞极化，发挥减轻UUO小鼠肾纤维化的作用。

关键词: 清肾颗粒, Akt3, 巨噬细胞极化, 肾纤维化

Abstract:

Objective To clarify whether Qingshen Granules (QSG) inhibits renal fibrosis by regulating Akt3-mediated macrophage polarization. Methods Adult C57BL/6 mice were randomized into Sham group, unilateral ureteral obstruction (UUO) model group, and UUO with QSG treatment group (n=6) for treatment with daily gavage of distilled water or QSG (4.0 g/kg) as indicated for 2 weeks. In AAV9 experiments, the mice received intrarenal injections of AAV9-shRNA(Akt3)-GFP for Akt3 knockdown or AAV9-shRNA-GFP (negative control) 2 weeks before sham operation or UUO modeling. After the treatments, the mice were examined for renal fibrosis, renal function, and macrophage polarization using HE staining, Masson staining, ELISA, Western blotting, RT-qPCR, immunohistochemistry, immunofluorescence staining, and flow cytometry. In the cell experiment, TGF‑β1-induced HK-2 cells were co-cultured with THP-1-derived macrophages, and the effects of QSG-medicated rat serum on cell viability, proliferation, and macrophage polarization were evaluated using CCK-8 and EdU assays, Western blotting and flow cytometry. Results Compared with the sham-operated mice, the UUO mice showed impaired renal function, renal tubular injury, collagen deposition, upregulated expressions of IL-6 and TNF-α mRNA and α-SMA protein, and downregulated E-cad protein expression, which were significantly improved by QSG treatment. In AAV9 experiments, the UUO mice with control virus injection showed obvious renal fibrosis and increased M1 macrophages, while AAV9-shRNA(Akt3)‑GFP injection significantly alleviated renal fibrosis and inhibited M1 macrophage polarization without affecting M2 macrophages. In the co-cultured cells, treatment with QSG-medicated serum significantly reversed TGF-β1-induced reduction of HK-2 cell viability and proliferation, upregulated Akt3 and α‑SMA expressions, downregulated E-cad expression, and inhibited M0-to-M1 polarization of THP-1 cells induced by TGF‑β1-treated HK-2 cells. Conclusion QSG alleviates renal fibrosis in UUO mice by inhibiting Akt3-mediated M1 macrophage polarization.

Key words: Qingshen Granules, Akt3, macrophage polarization, renal fibrosis

王伟丽, 高怡琳, 洪馨, 陈义珍, 程梦, 张磊, 戴荣, 王亿平. 清肾颗粒通过调控Akt3介导的M1型巨噬细胞极化改善单侧输尿管梗阻小鼠肾纤维化[J]. 南方医科大学学报, 2026, 46(6): 1216-1227.

Weili WANG, Yilin GAO, Xin HONG, Yizhen CHEN, Meng CHENG, Lei ZHANG, Rong DAI, Yiping WANG. Qingshen Granules alleviate renal fibrosis in mice with unilateral ureteral obstruction by regulating Akt3-mediated M1 macrophage polarization[J]. Journal of Southern Medical University, 2026, 46(6): 1216-1227.

图/表 9

表1 引物序列

Tab.1 Primer sequences (5' to 3') for RT-qPCR

Gene	Forwardprimer (5'→3')	Reverseprimer (5'→3')
Mo-β-actin	AGTGTGACGTTGACATCCGT	TGCTAGGAGCCAGAGCAGTA
Mo-TNF-α	CTCATGCACCACCATCAAGG	ACCTGACCACTCTCCCTTTG
Mo-IL-6	GGAGCCCACCAAGAACGATA	ACCAGCATCAGTCCCAAGAA
Mo-α-SMA	GTCCCAGACATCAGGGAGTAA	TCGGATACTTCAGCGTCAGGA
Mo-E-cad	GTCCTGGGCAGAGTGAGATT	CGTCTGTCGCCACTTTGAAT

图1 清肾颗粒改善UUO小鼠肾功能,减轻肾纤维化与炎症反应

Fig.1 Qingshen Granules (QSG) improve renal function and alleviate renal fibrosis in UUO mice. A, B: Results of HE staining and Masson staining of the renal tissues of the mice in each group (Scale bar=50 µm, n=6). C, D: Scr and BUN levels of the mice (n=6). E, F: RT-qPCR detection results of IL-6 and TNF-α mRNA in each group (n=6). *P<0.05 vs Sham group; #P<0.05 vs Model group.

图2 清肾颗粒对UUO小鼠肾组织中α-SMA、E-cad表达的影响

Fig. 2 Effect of QSG on expressions of α-SMA and E-cad in renal tissues of UUO mice. A-C: Western blotting for detecting α-SMA and E-cad expression levels in each group (n=3). D, E: RT-qPCR detection results of α-SMA and E-cad mRNA in each group (n=6). F-H: Immunohistochemical staining results for detecting renal expressions of α-SMA and E-cad (Scale bar=50 µm, n=6). *P<0.05 vs Sham group; #P<0.05 vs Model group.

图3 敲低Akt3表达减轻肾纤维化

Fig.3 Knockdown of Akt3 alleviates renal fibrosis in UUO mice. A, B: Western blotting for detecting Akt3 expression level in each group (n=3). C-E: Western blotting for detecting α-SMA and E-cad expression levels in each group (n=3). F-H: Results of immunofluorescence staining of α-SMA and E-cad in renal tissues of the mice in each group (Scale bar = 50 µm, n=6). *P<0.05 vs Sham+NC group; #P<0.05 vs Model+NC group.

图4 敲低Akt3表达抑制M1巨噬细胞极化

Fig.4 Knockdown of Akt3 expression inhibits M1 macrophage polarization. A-C: Flow cytometric analysis of M1/M2 macrophage expressions in the renal tissues of the mice in each group (n=3). *P<0.05 vs Sham+NC group; #P<0.05 vs Model+NC group.

图5 清肾颗粒主要入血成分与Akt3的分子对接结果

Fig.5 Molecular docking results of the major blood-absorbed components of QSG with Akt3. A: Heatmap of molecular docking binding energies for active components of QSG with binding energy <-5.0 kcal/mol against Akt3. B-F: Docking modes and binding site diagrams of Baicalin (B), Genistein 4'-O-glucuronide (C), Berberine (D), Rubiadin (E), and Apigenin (F) with Akt3.

图6 清肾颗粒下调Akt3表达,抑制M1巨噬细胞极化

Fig.6 QSG downregulates Akt3 expression and inhibits M1 macrophage polarization in the renal tissues of UUO mice. A, B: Western blotting for detecting Akt3 expression in each group (n=3). C-E: M1/M2 macrophage expression in the renal tissues of the mice in each group (n=3). *P<0.05 vs Sham group; #P<0.05 vs Model group.

图7 清肾颗粒含药血清下调Akt3表达,抑制 TGF-β1诱导的HK-2细胞纤维化

Fig.7 QSG-medicated serum inhibits Akt3 expression and TGF-β1-induced HK-2 cell fibrosis. A: Cell viability of cells in each group (n=6). B, C: EdU cell proliferation assay (Scale bar=100 μm, n=3). D-G: Western blotting for Akt3, α-SMA, and E-cad expressions in cells from each group (n=3). * P<0.05 vs Control group; #P<0.05 vs TGF-β1 group.

图8 清肾颗粒含药血清抑制 M1巨噬细胞极化

Fig.8 QSG-medicated serum inhibits M1 macrophage polarization. A-C: Flow cytometric analysis of M1/M2 macrophage expression levels in THP-1 cells from each group (n=3). *P<0.05 vs Control group; #P<0.05 vs TGF-β1 group.

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清肾颗粒通过调控Akt3介导的M1型巨噬细胞极化改善单侧输尿管梗阻小鼠肾纤维化

Qingshen Granules alleviate renal fibrosis in mice with unilateral ureteral obstruction by regulating Akt3-mediated M1 macrophage polarization

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