Xin-Ji-Er-Kang ameliorates kidney injury following myocardial infarction by inhibiting oxidative stress via Nrf2/HO-1 pathway in rats

Lian, Feng-zhen; Cheng, Pan; Ruan, Cheng-shao; Ling, Xin-xin; Wang, Xiaoyun; Pan, Min‐Hsiung; Chen, Mei‐Ling; Shen, Adong; Gao, Shan

doi:10.1016/j.biopha.2019.109124

Cited by 11 publications

(5 citation statements)

References 53 publications

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“…Nrf2, which is normally coupled to Keap1 and is confined to the cytoplasm, separates from it in times of oxidative stress and relocates to the nucleus. In the nucleus, Nrf2 binds to the antioxidant response elements (ARE) and affects the gene expression of antioxidant and detoxifying enzymes [53][54][55]. One of the important enzymes is the phase II detoxification enzymes such as HO-1 (downstream enzyme), SOD, CAT, and GPx, which play an important role in protecting the kidney against oxidative stress and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Platelet Rich Plasma and Adipose-Derived Mesenchymal Stem Cells Mitigate Methotrexate-Induced Nephrotoxicity in Rat via Nrf2/Pparγ/HO-1 and NF-Κb/Keap1/Caspase-3 Signaling Pathways: Oxidative Stress and Apoptosis Interplay

Wani

Ibrahim

Ameen

et al. 2023

Toxics

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Background: the nephrotoxicity of methotrexate (MTX) is observed in high-dose therapy. Moreover, low-dose MTX therapy for rheumatic diseases is debatable and claimed to cause renal impairment. This study aimed at studying the effect of methotrexate in repeated low doses on rat kidneys and assessing the efficacy of adipose-derived mesenchymal stem cells (AD-MSCs) and platelet rich plasma (PRP) for attenuating this effect. Methods: Forty-two male Wistar rats were used, 10 rats were donors of AD-MSCs and PRP, 8 rats served as control, and the remaining rats were subjected to induction of nephrotoxicity by MTX intraperitoneal injection once weekly for successive 8 weeks and then assigned into 3 groups of 8 animals each: Group II: received MTX only. Group III: received MTX + PRP. Group IV: received MTX + AD-MSCs. After one month, rats were anaesthetized, serum-sampled, and renal tissue removed for biochemical, histological, and ultrastructural evaluation. Results: there was significant tubular degeneration, glomerulosclerosis, fibrosis, decreased renal index, along with increased levels of urea and creatinine in the MTX group compared to the control group. Immunohistochemical expression of caspase-3 and iNOS in the renal tissue was significantly increased in group II compared to groups III and IV. Biochemical results revealed higher tissue malondialdehyde (MDA) concentration in the MTX-injected group which decreased significantly in co-treatment with either AD-MSC or PRP + MTX. MSC promoted the activation of the Nrf2/PPARγ/HO-1 and NF-κB/Keap1/caspase-3 pathways, increased antioxidant enzyme activities, reduced lipid peroxidation levels, and alleviated oxidative damage and apoptosis. PRP showed therapeutic effects and molecular mechanisms similar to MSC. Furthermore, MSC and PRP treatment significantly reduced MTX-induced upregulation of the pro-inflammatory (NF-κB, interleukin-1ß, and TNF-α), oxidative stress (Nrf-2, hemoxygenase-1, glutathione, and malondialdehyde), and nitrosative stress (iNOS) markers in the kidney. Conclusion: repeated administration of low-dose MTX resulted in massive renal tissue toxicity and deterioration of renal function in rats which proved to be attenuated by PRP and AD-MSCs through their anti-inflammatory, anti-apoptotic and anti-fibrotic properties.

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Section: Discussionmentioning

confidence: 99%

Platelet Rich Plasma and Adipose-Derived Mesenchymal Stem Cells Mitigate Methotrexate-Induced Nephrotoxicity in Rat via Nrf2/Pparγ/HO-1 and NF-Κb/Keap1/Caspase-3 Signaling Pathways: Oxidative Stress and Apoptosis Interplay

Wani

Ibrahim

Ameen

et al. 2023

Toxics

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“…According to Lian et al, in addition to downregulating the expression of several inflammatory factors and activating apoptosis-related proteins, MI model of rats having progressive nephropathy activate the renin-angiotensin-aldosterone system (RAAS), which is simultaneously connected with the defective Nrf2 pathway [42]. Hence, restoration of Nrf2 may have a positive influence on the RAAS.…”

Section: Myocardial Infarction (Mi)mentioning

confidence: 99%

“…[37] Rheumatic heart disease (RHD) Inhibits signal transducer [39] Cardiac tumors Regulates antioxidant defense enzymes and counteracts oxidative stress [40] Reduces toxicity with sulforaphane [41] Myocardial infarction (MI) Involved the renin-angiotensin-aldosterone system [42] Upgrades antioxidant genes [43] Myocardial ischemia reperfusion injury (MIRI)…”

Section: Viral Myocarditismentioning

confidence: 99%

The Nrf-2/HO-1 Signaling Axis: A Ray of Hope in Cardiovascular Diseases

Zhang

Lei

et al. 2020

Cardiology Research and Practice

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Cardiovascular disease, which can lead to angina and shortness of breath, remains one of the most serious threats to human health. Owing to its imperceptible symptoms, it is difficult to determine the pathogenesis and treatment methods for cardiovascular disease. Nuclear factor erythropoietin-2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) is a protein found in all cells of the human body. It is activated, transferred to the nucleus, and bound to DNA by antioxidant response elements (AREs). As a regulator of the antioxidant system, it upregulates the expression of HO-1 to reduce oxidative stress. Nrf2/HO-1 also has the ability to modulate calcium levels to prevent ferroptosis, pyroptosis, autophagy, programmed cell necrosis, alkaliptosis, and clockophagy. In view of the importance of Nrf2/HO-1 in the regulation of homeostasis, this review summarizes current research on the relationship between cardiovascular disease and Nrf2/HO-1. Normal cardiovascular diseases, such as viral myocarditis and myocardial ischemia-reperfusion injury, have been treated with Nrf2/HO-1. Rheumatic heart disease, cardiac tumors, arteriosclerosis, arrhythmia, hypertensive heart disease, and myocardial infarction have also been treated during experiments. Research has demonstrated the clinical application of Nrf2/HO-1 in pediatric cardiovascular disease; further clinical trials will help elucidate the potential of the Nrf2/HO-1 signaling axis.

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“…The therapeutic effect of Radix Scrophulariae on SHr can be attributed to the suppression of the raS through the inhibition of the extracellular regulated protein kinase 1/2, c-Jun n-terminal kinase and p38 MaPK pathways (58). Xin-Ji-er-Kang can inhibit oxidative stress by affecting the raS, and can improve renal injury after myocardial infarction in rats (59). in addition, all herbal medicines that contain flavonoids, terpenoids, saponins and alkaloids are able to inhibit the raS (16).…”

Section: Mechanism Of Herbal Medicine In the Treatment Of Hypertensive Nephropathymentioning

confidence: 99%

Mechanism of herbal medicine on hypertensive nephropathy (Review)

Dong

Dai

Feng³

et al. 2021

Mol Med Rep

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Hypertensive nephropathy is the most common complication of hypertension, and is one of the main causes of end-stage renal disease (ESRD) in numerous countries. The basic pathological feature of hypertensive nephropathy is arteriolosclerosis followed by renal parenchymal damage. The etiology of this disease is complex, and its pathogenesis is mainly associated with renal hemodynamic changes and vascular remodeling. Despite the increased knowledge on the pathogenesis of hypertensive nephropathy, the current clinical treatment methods are still not effective in preventing the development of the disease to ESRD. Herbal medicine, which is used to relieve symptoms, can improve hypertensive nephropathy through multiple targets. Since there are few clinical studies on the treatment of hypertensive nephropathy with herbal medicine, this article aims to review the progress on the basic research on the treatment of hypertensive nephropathy with herbal medicine, including regulation of the renin angiotensin system, inhibition of sympathetic excitation, antioxidant stress and anti-inflammatory protection of endothelial cells, and improvement of obesity-associated factors. Herbal medicine with different components plays a synergistic and multi-target role in the treatment of hypertensive nephropathy. The description of the mechanism of herbal medicine in the treatment of hypertensive nephropathy will contribute towards the progress of modern medicine.

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Xin-Ji-Er-Kang ameliorates kidney injury following myocardial infarction by inhibiting oxidative stress via Nrf2/HO-1 pathway in rats

Cited by 11 publications

References 53 publications

Platelet Rich Plasma and Adipose-Derived Mesenchymal Stem Cells Mitigate Methotrexate-Induced Nephrotoxicity in Rat via Nrf2/Pparγ/HO-1 and NF-Κb/Keap1/Caspase-3 Signaling Pathways: Oxidative Stress and Apoptosis Interplay

Platelet Rich Plasma and Adipose-Derived Mesenchymal Stem Cells Mitigate Methotrexate-Induced Nephrotoxicity in Rat via Nrf2/Pparγ/HO-1 and NF-Κb/Keap1/Caspase-3 Signaling Pathways: Oxidative Stress and Apoptosis Interplay

The Nrf-2/HO-1 Signaling Axis: A Ray of Hope in Cardiovascular Diseases

Mechanism of herbal medicine on hypertensive nephropathy (Review)

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