Journal of Traditional Chinese Medicine ›› 2024, Vol. 44 ›› Issue (2): 324-333.DOI: 10.19852/j.cnki.jtcm.20240203.001
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Protective effect of modified Huangqi Chifeng decoction (加味黄芪赤风汤) on immunoglobulin A nephropathy through toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-kappa B signaling pathway
LI Liusheng1,2, ZHAO Mingming3,4, CHANG Meiying3,4, SI Yuan3,4, ZHAO Jinning6, YANG Bin5(
), ZHANG Yu3,4()
- 1 Department of Oncology, Beijing Hospital of Integrated Traditional Chinese and Western Medicine, Beijing 100039, China
2 Department of Nephropathy, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China
3 Department of Nephropathy, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China
4 Xin-Huangpu Joint Innovation Institute of Chinese Medicine, Guangzhou 510070, China
5 Department of Pathology Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China
6 Department of Experimental Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China
-
Received:2022-12-09Accepted:2023-05-04Online:2024-04-15Published:2024-02-03 -
Contact:Prof. ZHANG Yu, Department of Nephropathy, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.zhangyu8225@126.com ; YANG Bin, Department of Pathology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.yangbin555@126.com Telephone: +86-13611079831 -
Supported by:Joint Innovation Fundation of JIICM: Health Management of Chronic Kidney Disease Based on Integrated Traditional Chinese And Western Medicine(2021IR009);Natural Science Foundation-funded Project: the Mechanism of Modified Huangqi Chifeng Decoction Protect Damaged Podocyte via Cross-Talking of PI3K/AKT/mTOR and AMPK/mTOR/ULK1 Signaling Pathway Regulate Autophapy(81873300);The Central Public-interest Scientific Institution Basal Research Fund of the China Academy of Chinese Medical Sciences: Comprehensive Evaluation of Clinical efficacy of Modified Huangqi Chifeng Decoction on IgA Nephropathy(ZZ11-023);The Beijing Municipal of Science and Technology Major Project: Evaluation of Clinical Efficacy of Modified Huangqi Chifeng Decoction in Treating Proteinuria in IgA Nephropathy Based on "Deficiency-Wind-Blood-Stasis-Toxicity" Mechanism in Chinese Medicine(Z191100006619063)
Cite this article
LI Liusheng, ZHAO Mingming, CHANG Meiying, SI Yuan, ZHAO Jinning, YANG Bin, ZHANG Yu. Protective effect of modified Huangqi Chifeng decoction (加味黄芪赤风汤) on immunoglobulin A nephropathy through toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-kappa B signaling pathway[J]. Journal of Traditional Chinese Medicine, 2024, 44(2): 324-333.
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Figure 1 MHCD reduced proteinuria A: proteinuria changes at the stage of model building (n of control group = 13, n of model group = 53). B: proteinuria changes during intervention (n = 10). The telmisartan group were intragastrically administered telmisartan at a dose of 8.33 mg·kg-1·d-1 for 8 weeks; The MHCD-H, MHCD-M, and MHCD-L groups were intragastrically administered MHCD at 25.0, 12.5, and 6.25 g·kg-1·d-1, respectively, for 8 weeks; The control group and model group were given the same volumes of normal saline for 8 weeks. MHCD: modified Huangqi Chifeng decoction; MHCD-L: low-dose modified Huangqi Chifeng decoction; MHCD-M: medium-dose modified Huangqi Chifeng decoction; MHCD-H: high-dose modified Huangqi Chifeng decoction. Data represent the mean ± standard deviation using one-way analysis of variance. aP < 0.01 vs control group; bP < 0.05 and cP < 0.01 vs model group; dP < 0.05 vs MHCD-M group, MHCD-H group and telmisartan group.
Figure 1 MHCD reduced proteinuria A: proteinuria changes at the stage of model building (n of control group = 13, n of model group = 53). B: proteinuria changes during intervention (n = 10). The telmisartan group were intragastrically administered telmisartan at a dose of 8.33 mg·kg-1·d-1 for 8 weeks; The MHCD-H, MHCD-M, and MHCD-L groups were intragastrically administered MHCD at 25.0, 12.5, and 6.25 g·kg-1·d-1, respectively, for 8 weeks; The control group and model group were given the same volumes of normal saline for 8 weeks. MHCD: modified Huangqi Chifeng decoction; MHCD-L: low-dose modified Huangqi Chifeng decoction; MHCD-M: medium-dose modified Huangqi Chifeng decoction; MHCD-H: high-dose modified Huangqi Chifeng decoction. Data represent the mean ± standard deviation using one-way analysis of variance. aP < 0.01 vs control group; bP < 0.05 and cP < 0.01 vs model group; dP < 0.05 vs MHCD-M group, MHCD-H group and telmisartan group.
Figure 2 MHCD decreased IgA deposition (n = 10, × 400) A1-A6: images of Immunofluorescence staining. B: quantitative analysis of IgA deposition. A1, A2: selected from the control group (A1) and the model group (A2) were given the same volumes of normal saline for 8 weeks; A3: selected from the telmisartan group were intragastrically administered telmisartan at a dose of 8.33 mg·kg-1·d-1 for 8 weeks; A4: selected from the MHCD-L group were intragastrically administered MHCD at 6.25 g·kg-1·d-1 for 8 weeks; A5: selected from the MHCD-M group were intragastrically administered MHCD at 12.5 g·kg-1·d-1 for 8 weeks; A6: selected from the MHCD-H group were intragastrically administered MHCD at 25.0 g·kg-1·d-1 for 8 weeks. The Data represent the mean ± standard deviation using one-way analysis of variance. aP < 0.01 vs control group; bP < 0.05 vs model group. MHCD: modified Huangqi Chifeng decoction; MHCD-L: low-dose modified Huangqi Chifeng decoction; MHCD-M: medium-dose modified Huangqi Chifeng decoction; MHCD-H: high-dose modified Huangqi Chifeng decoction.
Figure 2 MHCD decreased IgA deposition (n = 10, × 400) A1-A6: images of Immunofluorescence staining. B: quantitative analysis of IgA deposition. A1, A2: selected from the control group (A1) and the model group (A2) were given the same volumes of normal saline for 8 weeks; A3: selected from the telmisartan group were intragastrically administered telmisartan at a dose of 8.33 mg·kg-1·d-1 for 8 weeks; A4: selected from the MHCD-L group were intragastrically administered MHCD at 6.25 g·kg-1·d-1 for 8 weeks; A5: selected from the MHCD-M group were intragastrically administered MHCD at 12.5 g·kg-1·d-1 for 8 weeks; A6: selected from the MHCD-H group were intragastrically administered MHCD at 25.0 g·kg-1·d-1 for 8 weeks. The Data represent the mean ± standard deviation using one-way analysis of variance. aP < 0.01 vs control group; bP < 0.05 vs model group. MHCD: modified Huangqi Chifeng decoction; MHCD-L: low-dose modified Huangqi Chifeng decoction; MHCD-M: medium-dose modified Huangqi Chifeng decoction; MHCD-H: high-dose modified Huangqi Chifeng decoction.
Figure 3 MHCD downregulated the expressions of MCP-1, IL-6, and TGF-β1 A1-A6: images of immunohistochemistry of MCP-1 (× 200); B1-B6: images of immunohistochemistry of IL-6 (× 200); C1-C6: images of immunohistochemistry of TGF-β1 (× 200); D: quantitation of MCP-1 measured by immunohistochemistry; E: quantitation of IL-6 measured by immunohistochemistry; F: quantitation of TGF-β1 measured by immunohistochemistry; G: MCP-1 was measured by qPCR; H: IL-6 was measured by qPCR; I: TGF-β1 was measured by qPCR. A1, A2, B1, B2, C1, C2: selected from the control group (A1, B1, C1) and the model group (A2, B2, C2) were given the same volumes of normal saline for 8 weeks; A3, B3, C3: selected from the telmisartan group were intragastrically administered telmisartan at a dose of 8.33 mg·kg-1·d-1 for 8 weeks; A4, B4, C4: selected from the MHCD-L group were intragastrically administered MHCD at 6.25 g·kg-1·d-1 for 8 weeks; A5, B5, C5: selected from the MHCD-M group were intragastrically administered MHCD at 12.5 g·kg-1·d-1 for 8 weeks; A6, B6, C6: selected from the MHCD-H group were intragastrically administered MHCD at 25.0 g·kg-1·d-1 for 8 weeks. MCP-1: monocyte chemotactic protein 1; IL-6: interleukin 6; TGF-β1: transforming growth factor-β 1; MHCD: modified Huangqi Chifeng decoction; MHCD-L: low-dose modified Huangqi Chifeng decoction; MHCD-M: medium-dose modified Huangqi Chifeng decoction; MHCD-H: high-dose modified Huangqi Chifeng decoction. The Data represent the mean ± standard deviation using one-way analysis of variance (n = 10). aP < 0.01 vs control group; bP < 0.05 and cP < 0.01 vs model group.
Figure 3 MHCD downregulated the expressions of MCP-1, IL-6, and TGF-β1 A1-A6: images of immunohistochemistry of MCP-1 (× 200); B1-B6: images of immunohistochemistry of IL-6 (× 200); C1-C6: images of immunohistochemistry of TGF-β1 (× 200); D: quantitation of MCP-1 measured by immunohistochemistry; E: quantitation of IL-6 measured by immunohistochemistry; F: quantitation of TGF-β1 measured by immunohistochemistry; G: MCP-1 was measured by qPCR; H: IL-6 was measured by qPCR; I: TGF-β1 was measured by qPCR. A1, A2, B1, B2, C1, C2: selected from the control group (A1, B1, C1) and the model group (A2, B2, C2) were given the same volumes of normal saline for 8 weeks; A3, B3, C3: selected from the telmisartan group were intragastrically administered telmisartan at a dose of 8.33 mg·kg-1·d-1 for 8 weeks; A4, B4, C4: selected from the MHCD-L group were intragastrically administered MHCD at 6.25 g·kg-1·d-1 for 8 weeks; A5, B5, C5: selected from the MHCD-M group were intragastrically administered MHCD at 12.5 g·kg-1·d-1 for 8 weeks; A6, B6, C6: selected from the MHCD-H group were intragastrically administered MHCD at 25.0 g·kg-1·d-1 for 8 weeks. MCP-1: monocyte chemotactic protein 1; IL-6: interleukin 6; TGF-β1: transforming growth factor-β 1; MHCD: modified Huangqi Chifeng decoction; MHCD-L: low-dose modified Huangqi Chifeng decoction; MHCD-M: medium-dose modified Huangqi Chifeng decoction; MHCD-H: high-dose modified Huangqi Chifeng decoction. The Data represent the mean ± standard deviation using one-way analysis of variance (n = 10). aP < 0.01 vs control group; bP < 0.05 and cP < 0.01 vs model group.
Figure 4 MHCD inhibited the TLR4/MyD88/NF-κB signaling pathway A1-A6: images of immunohistochemistry of.TLR4 (× 200); B1-B6: images of immunohistochemistry of MyD88 (× 200); C1-C6: images of immunohistochemistry of NF-κB P65 (× 200); D: quantitation of TLR4 measured by immunohistochemistry; E: quantitation of MyD88 measured by immunohistochemistry; F: quantitation of NF-κB P65 measured by immunohistochemistry; G: images of TLR4, MyD88 and NF-κB P65 analyzed by Western blotting; H: TLR4 was analyzed by Western blotting; I: MyD88 was analyzed by Western blotting; J: NF-κB P65 was analyzed by Western blotting; K: TLR4 was analyzed by qPCR; L: MyD88 was analyzed by qPCR; M: NF-κB was analyzed by qPCR. A1, A2, B1, B2, C1, C2: selected from the control group (A1, B1, C1) and the model group (A2, B2, C2) were given the same volumes of normal saline for 8 weeks; A3, B3, C3: selected from the telmisartan group were intragastrically administered telmisartan at a dose of 8.33 mg·kg-1·d-1 for 8 weeks; A4, B4, C4: selected from the MHCD-L group were intragastrically administered MHCD at 6.25 g·kg-1·d-1 for 8 weeks; A5, B5, C5: selected from the MHCD-M group were intragastrically administered MHCD at 12.5 g·kg-1·d-1 for 8 weeks; A6, B6, C6: selected from the MHCD-H group were intragastrically administered MHCD at 25.0 g·kg-1·d-1 for 8 weeks. TLR4: toll-like receptor 4; MyD88: myeloid differentiation primary response 88; NF-κB: nuclear factor kappa-B; MHCD: modified Huangqi Chifeng decoction; MHCD-L: low-dose modified Huangqi Chifeng decoction; MHCD-M: medium-dose modified Huangqi Chifeng decoction; MHCD-H: high-dose modified Huangqi Chifeng decoction. The Data represent the mean ± standard deviation using one-way analysis of variance (n = 10). aP < 0.01 and dP < 0.05 vs control group; bP < 0.05 and cP < 0.01 vs model group.
Figure 4 MHCD inhibited the TLR4/MyD88/NF-κB signaling pathway A1-A6: images of immunohistochemistry of.TLR4 (× 200); B1-B6: images of immunohistochemistry of MyD88 (× 200); C1-C6: images of immunohistochemistry of NF-κB P65 (× 200); D: quantitation of TLR4 measured by immunohistochemistry; E: quantitation of MyD88 measured by immunohistochemistry; F: quantitation of NF-κB P65 measured by immunohistochemistry; G: images of TLR4, MyD88 and NF-κB P65 analyzed by Western blotting; H: TLR4 was analyzed by Western blotting; I: MyD88 was analyzed by Western blotting; J: NF-κB P65 was analyzed by Western blotting; K: TLR4 was analyzed by qPCR; L: MyD88 was analyzed by qPCR; M: NF-κB was analyzed by qPCR. A1, A2, B1, B2, C1, C2: selected from the control group (A1, B1, C1) and the model group (A2, B2, C2) were given the same volumes of normal saline for 8 weeks; A3, B3, C3: selected from the telmisartan group were intragastrically administered telmisartan at a dose of 8.33 mg·kg-1·d-1 for 8 weeks; A4, B4, C4: selected from the MHCD-L group were intragastrically administered MHCD at 6.25 g·kg-1·d-1 for 8 weeks; A5, B5, C5: selected from the MHCD-M group were intragastrically administered MHCD at 12.5 g·kg-1·d-1 for 8 weeks; A6, B6, C6: selected from the MHCD-H group were intragastrically administered MHCD at 25.0 g·kg-1·d-1 for 8 weeks. TLR4: toll-like receptor 4; MyD88: myeloid differentiation primary response 88; NF-κB: nuclear factor kappa-B; MHCD: modified Huangqi Chifeng decoction; MHCD-L: low-dose modified Huangqi Chifeng decoction; MHCD-M: medium-dose modified Huangqi Chifeng decoction; MHCD-H: high-dose modified Huangqi Chifeng decoction. The Data represent the mean ± standard deviation using one-way analysis of variance (n = 10). aP < 0.01 and dP < 0.05 vs control group; bP < 0.05 and cP < 0.01 vs model group.
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