Ginsenoside Rg1 attenuates LPS-induced chronic renal injury by inhibiting NOX4-NLRP3 signaling in mice
Chronic renal injury (CRI) is a common pathological damage in chronic renal disease, and the therapeutic options for preventing its progression are limited at present. Ginsenoside Rg1 (Rg1) is reported to have a protective effect on renal injury by improving oxidative stress and inflammation. Lipopo...
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Elsevier
2022-06-01
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| Series: | Biomedicine & Pharmacotherapy |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0753332222003250 |
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| author | Duoduo Zhang Pengmin Ji Ran Sun Huimin Zhou Lei Huang Liangliang Kong Weiping Li Weizu Li |
| author_facet | Duoduo Zhang Pengmin Ji Ran Sun Huimin Zhou Lei Huang Liangliang Kong Weiping Li Weizu Li |
| author_sort | Duoduo Zhang |
| collection | DOAJ |
| description | Chronic renal injury (CRI) is a common pathological damage in chronic renal disease, and the therapeutic options for preventing its progression are limited at present. Ginsenoside Rg1 (Rg1) is reported to have a protective effect on renal injury by improving oxidative stress and inflammation. Lipopolysaccharide (LPS) plays important roles in inducing inflammatory and high-dose LPS is often used to perform acute renal injury. However, little is known about the effect of low-dose LPS on CRI, and the protective effect of Rg1 against chronic LPS-induced CRI. Here, we reported the protective effect and mechanism of Rg1 against LPS-induced CRI in mice. In this study, the results demonstrated that low-dose LPS (0.25 mg/kg) exposure for 14 days significantly induced renal function impairment and renal injury and fibrosis. Meanwhile, LPS exposure significantly increased reactive oxygen species (ROS) generation, NADPH oxidase 4 (NOX4) and NLRP3 inflammasome expression in renal cortex. However, treatment with Rg1, tempol (a superoxide dismutase mimetic), and apocynin (a NOX inhibitor) significantly improved renal function impairment and renal fibrosis, and significantly decreased the levels of TGF-β, IL-1β, KIM-1, β-Gal, and collagen IV in the kidneys. And Rg1 treatment also significantly reduced ROS generation and inhibited the activation of NOX4 and NLRP3 inflammasome. Overall, these results suggest that Rg1 treatment can ameliorate LPS-induced chronic kidney injury and renal fibrosis, the mechanisms may be involved in reducing NOX2-mediated oxidative stress and inhibiting NLRP1 inflammasome. |
| first_indexed | 2024-04-12T17:15:57Z |
| format | Article |
| id | doaj.art-7215dff226e94ee9ac372f9eb17a61fa |
| institution | Directory Open Access Journal |
| issn | 0753-3322 |
| language | English |
| last_indexed | 2024-04-12T17:15:57Z |
| publishDate | 2022-06-01 |
| publisher | Elsevier |
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| series | Biomedicine & Pharmacotherapy |
| spelling | doaj.art-7215dff226e94ee9ac372f9eb17a61fa2022-12-22T03:23:39ZengElsevierBiomedicine & Pharmacotherapy0753-33222022-06-01150112936Ginsenoside Rg1 attenuates LPS-induced chronic renal injury by inhibiting NOX4-NLRP3 signaling in miceDuoduo Zhang0Pengmin Ji1Ran Sun2Huimin Zhou3Lei Huang4Liangliang Kong5Weiping Li6Weizu Li7Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei 230032, Anhui, China; Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, ChinaKey Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei 230032, Anhui, China; Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, ChinaKey Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei 230032, Anhui, China; Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, ChinaKey Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei 230032, Anhui, China; Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, ChinaKey Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei 230032, Anhui, China; Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, ChinaKey Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei 230032, Anhui, China; Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, ChinaKey Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei 230032, Anhui, China; Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, China; Anqing Medical and Pharmaceutical College, Anqing 246052, Anhui, China; Corresponding authors at: Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, China.Key Laboratory of Anti-Inflammatory and Immunopharmacology, Ministry of Education, Hefei 230032, Anhui, China; Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, China; Corresponding authors at: Department of Pharmacology, Basic Medicine College, Anhui Medical University, Hefei 230032, Anhui, China.Chronic renal injury (CRI) is a common pathological damage in chronic renal disease, and the therapeutic options for preventing its progression are limited at present. Ginsenoside Rg1 (Rg1) is reported to have a protective effect on renal injury by improving oxidative stress and inflammation. Lipopolysaccharide (LPS) plays important roles in inducing inflammatory and high-dose LPS is often used to perform acute renal injury. However, little is known about the effect of low-dose LPS on CRI, and the protective effect of Rg1 against chronic LPS-induced CRI. Here, we reported the protective effect and mechanism of Rg1 against LPS-induced CRI in mice. In this study, the results demonstrated that low-dose LPS (0.25 mg/kg) exposure for 14 days significantly induced renal function impairment and renal injury and fibrosis. Meanwhile, LPS exposure significantly increased reactive oxygen species (ROS) generation, NADPH oxidase 4 (NOX4) and NLRP3 inflammasome expression in renal cortex. However, treatment with Rg1, tempol (a superoxide dismutase mimetic), and apocynin (a NOX inhibitor) significantly improved renal function impairment and renal fibrosis, and significantly decreased the levels of TGF-β, IL-1β, KIM-1, β-Gal, and collagen IV in the kidneys. And Rg1 treatment also significantly reduced ROS generation and inhibited the activation of NOX4 and NLRP3 inflammasome. Overall, these results suggest that Rg1 treatment can ameliorate LPS-induced chronic kidney injury and renal fibrosis, the mechanisms may be involved in reducing NOX2-mediated oxidative stress and inhibiting NLRP1 inflammasome.http://www.sciencedirect.com/science/article/pii/S0753332222003250Ginsenoside Rg1LipopolysaccharideChronic renal injuryNLRP3 inflammasomeNADPH oxidase 4 |
| spellingShingle | Duoduo Zhang Pengmin Ji Ran Sun Huimin Zhou Lei Huang Liangliang Kong Weiping Li Weizu Li Ginsenoside Rg1 attenuates LPS-induced chronic renal injury by inhibiting NOX4-NLRP3 signaling in mice Biomedicine & Pharmacotherapy Ginsenoside Rg1 Lipopolysaccharide Chronic renal injury NLRP3 inflammasome NADPH oxidase 4 |
| title | Ginsenoside Rg1 attenuates LPS-induced chronic renal injury by inhibiting NOX4-NLRP3 signaling in mice |
| title_full | Ginsenoside Rg1 attenuates LPS-induced chronic renal injury by inhibiting NOX4-NLRP3 signaling in mice |
| title_fullStr | Ginsenoside Rg1 attenuates LPS-induced chronic renal injury by inhibiting NOX4-NLRP3 signaling in mice |
| title_full_unstemmed | Ginsenoside Rg1 attenuates LPS-induced chronic renal injury by inhibiting NOX4-NLRP3 signaling in mice |
| title_short | Ginsenoside Rg1 attenuates LPS-induced chronic renal injury by inhibiting NOX4-NLRP3 signaling in mice |
| title_sort | ginsenoside rg1 attenuates lps induced chronic renal injury by inhibiting nox4 nlrp3 signaling in mice |
| topic | Ginsenoside Rg1 Lipopolysaccharide Chronic renal injury NLRP3 inflammasome NADPH oxidase 4 |
| url | http://www.sciencedirect.com/science/article/pii/S0753332222003250 |
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