Rhein Inhibits NF-κB Signaling Pathway to Alleviate Inflammatory Response and Oxidative Stress of Rats with Chronic Glomerulonephritis

Objective. To explore the effect and mechanism of rhein on chronic glomerulonephritis (CGN). Method. Twenty-four eight-week-old male SD rats were randomly divided into following 4 groups (6 rats in each group): control group, CGN group, rhein group, and benazepril (Ben) group. And 5 mg/mL of cationi...

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Main Authors: Qian Chen, Hai Guo, JuanJuan Hu, Xiaofeng Zhao
Format: Article
Language:English
Published: Wiley 2022-01-01
Series:Applied Bionics and Biomechanics
Online Access:http://dx.doi.org/10.1155/2022/9671759
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author Qian Chen
Hai Guo
JuanJuan Hu
Xiaofeng Zhao
author_facet Qian Chen
Hai Guo
JuanJuan Hu
Xiaofeng Zhao
author_sort Qian Chen
collection DOAJ
description Objective. To explore the effect and mechanism of rhein on chronic glomerulonephritis (CGN). Method. Twenty-four eight-week-old male SD rats were randomly divided into following 4 groups (6 rats in each group): control group, CGN group, rhein group, and benazepril (Ben) group. And 5 mg/mL of cationization-bovine serum albumin (C-BSA) was mixed with an equal volume of Freund’s incomplete adjuvant for the preparation of 2.5 mg/mL of C-BSA solution. The rat model of CGN was established by injection of C-BSA for six weeks. Calculation of the renal index in rats was conducted. Biochemical detection was performed to measure the level of 24 h urinary protein, blood urea nitrogen (BUN), serum creatinine (SCr), and serum albumin (ALB) of the rats, as well as the level of malondiadehyde (MDA), superoxide (SOD), and glutathione peroxidase (GSH-Px) in the kidney tissue. Hematoxylin and eosin (H&E) staining was utilized to measure histological changes in the kidney of the rats. The level of TNF-α, IL-1β, IL-6, and ICAM-1 in rat kidney tissues was determined by enzyme-linked immunosorbent assay (ELISA). Western blot was applied to check the expression of NF-κB in the nucleus and cytoplasm as well as the expression of IκBα and p-IκBα in rat kidney tissues. Results. Rhein could decline urinary protein, restore blood biochemical parameters, and protect renal tissue in rats with CGN. Besides, rhein could inhibit the activity of the NF-κB signaling pathway in rats with CGN and could alleviate the inflammatory response and oxidative stress level at the same time. Conclusion. Rhein alleviates inflammatory responses and oxidative stress in rats with CGN. It also provides a theoretical basis and data support for the therapeutic drugs for CGN.
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spelling doaj-art-570192d766004d938f903d25efa87e9f2025-02-03T01:22:46ZengWileyApplied Bionics and Biomechanics1754-21032022-01-01202210.1155/2022/9671759Rhein Inhibits NF-κB Signaling Pathway to Alleviate Inflammatory Response and Oxidative Stress of Rats with Chronic GlomerulonephritisQian Chen0Hai Guo1JuanJuan Hu2Xiaofeng Zhao3Department of Traditional Chinese MedicineDepartment of Traditional Chinese MedicineDepartment of NephrologyDepartment of Traditional Chinese MedicineObjective. To explore the effect and mechanism of rhein on chronic glomerulonephritis (CGN). Method. Twenty-four eight-week-old male SD rats were randomly divided into following 4 groups (6 rats in each group): control group, CGN group, rhein group, and benazepril (Ben) group. And 5 mg/mL of cationization-bovine serum albumin (C-BSA) was mixed with an equal volume of Freund’s incomplete adjuvant for the preparation of 2.5 mg/mL of C-BSA solution. The rat model of CGN was established by injection of C-BSA for six weeks. Calculation of the renal index in rats was conducted. Biochemical detection was performed to measure the level of 24 h urinary protein, blood urea nitrogen (BUN), serum creatinine (SCr), and serum albumin (ALB) of the rats, as well as the level of malondiadehyde (MDA), superoxide (SOD), and glutathione peroxidase (GSH-Px) in the kidney tissue. Hematoxylin and eosin (H&E) staining was utilized to measure histological changes in the kidney of the rats. The level of TNF-α, IL-1β, IL-6, and ICAM-1 in rat kidney tissues was determined by enzyme-linked immunosorbent assay (ELISA). Western blot was applied to check the expression of NF-κB in the nucleus and cytoplasm as well as the expression of IκBα and p-IκBα in rat kidney tissues. Results. Rhein could decline urinary protein, restore blood biochemical parameters, and protect renal tissue in rats with CGN. Besides, rhein could inhibit the activity of the NF-κB signaling pathway in rats with CGN and could alleviate the inflammatory response and oxidative stress level at the same time. Conclusion. Rhein alleviates inflammatory responses and oxidative stress in rats with CGN. It also provides a theoretical basis and data support for the therapeutic drugs for CGN.http://dx.doi.org/10.1155/2022/9671759
spellingShingle Qian Chen
Hai Guo
JuanJuan Hu
Xiaofeng Zhao
Rhein Inhibits NF-κB Signaling Pathway to Alleviate Inflammatory Response and Oxidative Stress of Rats with Chronic Glomerulonephritis
Applied Bionics and Biomechanics
title Rhein Inhibits NF-κB Signaling Pathway to Alleviate Inflammatory Response and Oxidative Stress of Rats with Chronic Glomerulonephritis
title_full Rhein Inhibits NF-κB Signaling Pathway to Alleviate Inflammatory Response and Oxidative Stress of Rats with Chronic Glomerulonephritis
title_fullStr Rhein Inhibits NF-κB Signaling Pathway to Alleviate Inflammatory Response and Oxidative Stress of Rats with Chronic Glomerulonephritis
title_full_unstemmed Rhein Inhibits NF-κB Signaling Pathway to Alleviate Inflammatory Response and Oxidative Stress of Rats with Chronic Glomerulonephritis
title_short Rhein Inhibits NF-κB Signaling Pathway to Alleviate Inflammatory Response and Oxidative Stress of Rats with Chronic Glomerulonephritis
title_sort rhein inhibits nf κb signaling pathway to alleviate inflammatory response and oxidative stress of rats with chronic glomerulonephritis
url http://dx.doi.org/10.1155/2022/9671759
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AT juanjuanhu rheininhibitsnfkbsignalingpathwaytoalleviateinflammatoryresponseandoxidativestressofratswithchronicglomerulonephritis
AT xiaofengzhao rheininhibitsnfkbsignalingpathwaytoalleviateinflammatoryresponseandoxidativestressofratswithchronicglomerulonephritis