Evaluation of Antioxidant and Immunity Activities of Quercetin in Isoproterenol-Treated Rats

Liu, Hui; Zhang, Lei; Lu, Shaoping

doi:10.3390/molecules17044281

Cited by 63 publications

(37 citation statements)

References 40 publications

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“…Quercetin supplementation alone did not show any significant change but prevented the decline in GR activity in combined treatment group. The neuroprotective activity of quercetin has been attributed to its antioxidant properties whereby quercetin is reported to trigger the activity of GR, which increases the overall GSH content, thus strengthening the antioxidant defense system [49].…”

Section: Resultsmentioning

confidence: 99%

Neuroprotective Role of Quercetin against Arsenic Induced Oxidative Stress in Rat Brain

Nirankari¹,

Kamal

Dhawan

2016

J Environ Anal Toxicol

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Section: Resultsmentioning

confidence: 99%

Neuroprotective Role of Quercetin against Arsenic Induced Oxidative Stress in Rat Brain

Nirankari¹,

Kamal

Dhawan

2016

J Environ Anal Toxicol

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“…14) Studies have revealed a role for quercetin in reducing pancreatic oxidative stress during diabetes. 15) Quercetin was also shown to attenuate inflammation via inhibiting the NF-κB pathway and nitric oxide (NO)/inducible nitric oxide synthase (iNOS) system, [16][17][18] which suggests that it may potentially be an alternative treatment for insulin resistance in diabetes. However, there are few studies on the effects of quercetin on insulin resistance in skeletal muscle, and it has been suggested that quercetin promotes basal glucose uptake in C2C12 cells via AMPK activation as the mechanism behind the insulin-sensitizing effects.…”

mentioning

confidence: 99%

Quercetin But Not Quercitrin Ameliorates Tumor Necrosis Factor-Alpha-Induced Insulin Resistance in C2C12 Skeletal Muscle Cells

Dai

Ding

Zhang

et al. 2013

Biological & Pharmaceutical Bulletin

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Skeletal muscle is a major site for glucose metabolism and its injury by cytokines can induce insulin resistance leading to type 2 diabetes. It has been suggested that quercetin may act as an anti-diabetic agent, however, the effects of quercetin on insulin resistance in skeletal muscle remain unknown. We aimed to investigate the role of quercetin and its glycoside, quercitrin in tumor necrosis factor-alpha (TNF-α) induced C2C12 skeletal muscle cell impairment. Quercetin, but not quercitrin moderately attenuated the effects of TNF-α and enhanced the basal and insulin stimulated uptake of glucose in a dose-dependent manner via the activation of the protein kinase B (Akt) and AMP-activated protein kinase (AMPK) pathways. Furthermore, the underlying mechanism also involved the suppression of nuclear factor-κB (NF-κB) signaling and the nitric oxide (NO)/inducible nitric oxide synthase (iNOS) system, downstream of AMPK transduction. In summary, quercetin exhibited its effect of improving glucose uptake and insulin sensitivity in skeletal muscle cells via the two independent signaling pathways of Akt and AMPK, and can be developed as a potential anti-diabetic agent.Key words skeletal muscle cell; insulin resistance; quercetin; inflammation; AMP-activated protein kinase Type 2 diabetes is characterized by low-grade systemic inflammation, 1) and elevated levels of circulating proinflammatory mediators may lead to the process of insulin resistance, a critical issue for understanding the mechanisms that contribute to type 2 diabetes.2,3) Cytokines like tumor necrosis factor-alpha (TNF-α) directly bind to their receptor(s) on muscle cells or hepatocytes, interfere with intracellular insulin signaling by converging on common signaling routes like the nuclear factor-κB (NF-κB) pathway, and eventually dampen the cellular response to insulin. [3][4][5] Skeletal muscle is recognized as the major tissue for glucose metabolism, taking up nearly three quarters of insulin stimulated glucose uptake in the entire body.6) There are at least two major mechanisms for the uptake of glucose by glucose transporter 4 (Glut4) in skeletal muscle: one is an insulin-dependent phosphoinositide 3 (PI3) kinase and protein kinase B (Akt) pathway, while the other is an AMP-activated protein kinase (AMPK) signaling pathway stimulated by metabolic stress. 7,8) The serine/threonine kinase Akt, also known as protein kinase B (PKB) is a pivotal node in cell signaling downstream of growth factors, cytokines and other stimuli. 9)Cytokines may also affect insulin independent pathways regulating glucose disposal such as inhibiting the activation of AMPK.10) AMPK is a fuel-sensing enzyme, the phosphorylation of which regulates glucose uptake. 11) However, its role in skeletal muscle remains unclear. 12,13)Dietary compounds with anti-inflammatory properties that affect insulin sensitivity may be promising candidates for manipulating skeletal muscle insulin resistance for their low side effects and readily available natural sources. Quercetin (3,5,7,3′,4′-penta...

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“…Elevated levels of TBARS and lipid hydroperoxides in the heart and heart mitochondria decreased the membrane fluidity and altered membrane permeability which uncouples oxidative phosphorylation. [16] ISO-treated cardiotoxic rodent (Group 3) demonstrated expanded levels of LPO in the heart which could be credited to the amassing of ROS in the heart and irreversible harm to the myocardial membrane. [17] Activated LPO is an essential pathogenic occasion in MI, and the levels of lipid peroxide indicate the extent of infection.…”

Section: Resultsmentioning

confidence: 99%

Untitled

Uthamaramasamy¹

2017

IJGP

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Background: Mitochondrial lipids are essential for the mitochondrial architecture, the activity of respiratory proteins, and the transport of proteins into the mitochondria. Aim: In this study, the preventive role of Zanthoxylum armatum fruit on mitochondrial lipids alteration induced by isoproterenol hydrochloride (ISO) was evaluated in myocardial infarcted (MI) rats. Methods: Oral pre-treatment with hydroethanolic extract of Z. armatum fruit to ISO-induced rats was done for 30 days followed by the isolation of mitochondria from the heart tissue. The lipids such as total cholesterol (TC), phospholipids (PL), triglycerides (TG), and free fatty acids (FFA) in the heart mitochondria and lipid hydroperoxides and thiobarbituric acid reactive substances (TBARS) in the heart tissue were evaluated. Results: ISO-induced MI rats showed a significantly (P < 0.05) increased mitochondrial TC, TG, and FFA with a subsequent decrease in PL. Significantly increased levels of lipid hydroperoxides and TBARS were observed in the heart tissue of ISO-treated rats. Oral pre-treatment with hydroethanolic extract of Z. armatum fruit to ISO-induced rats significantly (P < 0.05) reverted these alterations near to normal status. Conclusion: Pretreatment with Z. armatum fruit favorably restored the biochemical alterations demonstrating that Z. armatum fruit has a significant protective effect on cardiac mitochondrial function against ISO-induced MI in rats.

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Evaluation of Antioxidant and Immunity Activities of Quercetin in Isoproterenol-Treated Rats

Cited by 63 publications

References 40 publications

Neuroprotective Role of Quercetin against Arsenic Induced Oxidative Stress in Rat Brain

Neuroprotective Role of Quercetin against Arsenic Induced Oxidative Stress in Rat Brain

Quercetin But Not Quercitrin Ameliorates Tumor Necrosis Factor-Alpha-Induced Insulin Resistance in C2C12 Skeletal Muscle Cells

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