Antioxidant effects and mechanism of silymarin in oxidative stress induced cardiovascular diseases

Taleb, Abdoh; Ahmad, Khalil; Ihsan, Awais Ullah; Qu, Jia; Lin, Na; Hezam, Kamal; Koju, Nirmala; Lei, Hui; Ding, Qi

doi:10.1016/j.biopha.2018.03.140

Cited by 150 publications

(98 citation statements)

References 152 publications

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“…A significant decrease in antioxidant enzyme (i.e., SOD CAT GPx, GR, and GST) activity levels were observed in DC and DC + ISO rats. Cardiac SOD catalyzes the dismutation of superoxide anion (O 2 − ) into hydrogen peroxide (H 2 O 2 ) and molecular oxygen (Taleb et al, ). SOD plays vital role in protection of cellular and histological damage produced by ROS.…”

Section: Discussionmentioning

confidence: 99%

The protective effect of kaempferol on heart via the regulation of Nrf2, NF‐κβ, and PI3K/Akt/GSK‐3β signaling pathways in isoproterenol‐induced heart failure in diabetic rats

Zhang

Guo

Wang

et al. 2019

Drug Development Research

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This study was designed to delineate the effect of kaempferol (KF) on heart failure (HF) in diabetic rats. Streptozotocin‐induced male diabetic rats received KF orally at 10 and 20 mg/kg for 42 consecutive days. In last 2 days of the experimental period, isoproterenol was subcutaneously injected at 85 mg/kg to induce HF. The hearts were processed for hemodynamic, biochemical, molecular, and histological investigations. Systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure were elevated in KF‐treated HF‐induced diabetic rats. Moreover, KF treatment resulted in decreased fasting blood glucose and glycosylated hemoglobin levels with increased serum insulin levels. Besides, serum cardiac injury markers like troponin‐I, creatine kinase‐muscle/brain, lactate dehydrogenase, and brain natriuretic peptide levels were significantly reduced in KF treatment. KF treatment has shown decrease in cardiac heme oxygenase‐1, nuclear factor erythroid 2–related factor 2 (Nrf‐2), and γ‐glutamylcysteine synthetase with increased Keap1 mRNA levels. The cardioprotection of KF was improved by inhibition of apoptosis via blocking phosphorylation of Akt/glycogen synthase kinase (GSK)‐3β and p38 mitogen‐activated protein‐kinase/extracellular signal‐regulated kinases signaling pathways in HF‐induced diabetic rats. Moreover, reduced cardiac apoptosis in KF treatment was confirmed by decreased terminal deoxynucleotidyl transferase dUTP nick‐end labeling (TUNEL) positive cells, histopathological changes in HF‐induced diabetic rats. Therefore, the cardioprotective effect of KF is attributed to the regulation of Nrf2, nuclear factor kappa‐light‐chain‐enhancer of activated B cells, and Akt/GSK‐3β signaling pathways in HF‐induced diabetic rats.

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Section: Discussionmentioning

confidence: 99%

The protective effect of kaempferol on heart via the regulation of Nrf2, NF‐κβ, and PI3K/Akt/GSK‐3β signaling pathways in isoproterenol‐induced heart failure in diabetic rats

Zhang

Guo

Wang

et al. 2019

Drug Development Research

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“…It has been known for years that vascular and cardiac tissues are rich sources of ROS, and smooth muscle cells and fibroblasts produce the majority of O 2 ⋅found in the normal vessel wall [17]. ROS are implicated in the pathogenesis of vascular injury diseases [18]. It was reported that plasma ET-1 levels were significantly increased in patients with pulmonary hypertension and that increased ET-1 binding to smooth muscle cell receptors resulted in persistent elevation of ROS levels, further aggravating vascular damage [19].…”

Section: Introductionmentioning

confidence: 99%

Endothelin-1 Downregulates Sulfur Dioxide/Aspartate Aminotransferase Pathway via Reactive Oxygen Species to Promote the Proliferation and Migration of Vascular Smooth Muscle Cells

Tian

Zhang

Huang

et al. 2020

Oxidative Medicine and Cellular Longevity

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The regulatory mechanisms for proliferation and migration of vascular smooth muscle cells have not yet been clear. The present study was designed to investigate whether and how endothelin-1 (ET-1) impacted the generation of endogenous sulfur dioxide (SO2) in rat vascular smooth muscle cell (VSMC) proliferation and migration. Primary VSMCs and purified aspartate aminotransferase (AAT) protein were used in this study. We found that in the presence of ET-1, the expression of PCNA and Ki-67 was upregulated and the migration of VSMCs was promoted, while the AAT activity and SO2 levels in VSMCs were reduced without any changes in AAT1 and AAT2 expression. SO2 supplementation successfully prevented the ET-1-facilitated expression of PCNA and Ki-67 and the migration of VSMCs. Interestingly, ET-1 significantly increased reactive oxygen species (ROS) production in association with SO2/AAT pathway downregulation in VSMCs compared with controls, while the ROS scavenger N-acetyl-L-cysteine (NAC) and the antioxidant glutathione (GSH) significantly abolished the ET-1-stimulated downregulation of the SO2/AAT pathway. Moreover, the AAT activity was reduced in purified protein after the treatment for 2 h. However, NAC and GSH blocked the hydrogen peroxide-induced AAT activity reduction. In conclusion, our results suggest that ET-1 results in the downregulation of the endogenous SO2/AAT pathway via ROS generation to enhance the proliferation and migration of VSMCs.

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“…It is a combination of silydianine, silychristine, silibinin and isosilybinin (11). Previous studies have shown that silymarin has antioxidant and anti-inflammatory properties (12,13). This research was aimed to assess the noxious effect of DIC intoxication on the liver through serum biochemical markers, oxidative stress, gene expression of tumor necrosis factor-α (TNF-α), histological alterations and protective role of silymarin on DIC intoxication in rats.…”

Section: Introductionmentioning

confidence: 99%

Silymarin mitigates diclofenac-induced liver toxicity through inhibition of inflammation and oxidative stress in male rats

Ramezannezhad

Nouri

Heidarian

2019

J Herbmed Pharmacol

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The present study showed that silymarin mitigates DIC-induced liver toxicity through inhibition of inflammation and oxidative stress in male rats. After clinical trials, silymarin may be used with DIC as a complementary drug for decreasing the toxicity of DIC.Please cite this paper as: Ramezannezhad P, Nouri A, Heidarian E. Silymarin mitigates diclofenac-induced liver toxicity through inhibition of inflammation and oxidative stress in male rats.

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Antioxidant effects and mechanism of silymarin in oxidative stress induced cardiovascular diseases

Cited by 150 publications

References 152 publications

The protective effect of kaempferol on heart via the regulation of Nrf2, NF‐κβ, and PI3K/Akt/GSK‐3β signaling pathways in isoproterenol‐induced heart failure in diabetic rats

The protective effect of kaempferol on heart via the regulation of Nrf2, NF‐κβ, and PI3K/Akt/GSK‐3β signaling pathways in isoproterenol‐induced heart failure in diabetic rats

Endothelin-1 Downregulates Sulfur Dioxide/Aspartate Aminotransferase Pathway via Reactive Oxygen Species to Promote the Proliferation and Migration of Vascular Smooth Muscle Cells

Silymarin mitigates diclofenac-induced liver toxicity through inhibition of inflammation and oxidative stress in male rats

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