Hesperetin rescues retinal oxidative stress, neuroinflammation and apoptosis in diabetic rats

Kumar, Binay; Gupta, Suresh; Srinivasan, B.P.; Nag, Tapas Chandra; Srivastava, Sushma; Saxena, Rohit; Jha, Kumar Abhiram

doi:10.1016/j.mvr.2013.01.002

Cited by 134 publications

(93 citation statements)

References 44 publications

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“…Epidemiological studies have shown that increased daily hesperetin intake reduces human mortal-ity from cardiovascular diseases, lung cancer and asthma [11] . Accumulating studies demonstrate that hesperetin is effective in treating many disorders because it exerts a wide range of biological effects, including vasorelaxation effects [12] , antioxidant effects [13] , neuroprotective effects [14] , anti-inflammatory effects [15] , antiviral effects and cholesterol-lowering effects [16] . However, reports on the effects of hesperetin on ion channels are sparse.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effects of hesperetin on Nav1.5 channels stably expressed in HEK 293 cells and on the voltage-gated cardiac sodium current in human atrial myocytes

Wang

Zhang

et al. 2016

Acta Pharmacol Sin

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Aim: Voltage-gated sodium channels composed of a pore-forming α subunit and auxiliary β subunits are responsible for the upstroke of the action potential in cardiac myocytes. The pore-forming subunit of the cardiac sodium channel Nav1.5, which is encoded by SCN5A, is the main ion channel that conducts the voltage-gated cardiac sodium current (I Na ) in cardiac cells. The current study sought to investigate the inhibitory effects of hesperetin on human cardiac Nav1.5 channels stably expressed in human embryonic kidney 293 (HEK 293) cells and on the voltage-gated cardiac sodium current (I Na ) in human atrial myocytes. Methods: The effects of hesperetin on human cardiac Nav1.5 channels expressed in HEK 293 cells and on cardiac Na + currents in human atrial myocytes were examined through whole-cell patch-clamp techniques. Results: Nav1.5 currents were potently and reversibly suppressed in a concentration-and voltage-dependent manner by hesperetin, which exhibited an IC 50 of 62.99 μmol/L. Hesperetin significantly and negatively shifted the voltage-dependent activation and inactivation curves. Hesperetin also markedly decelerated Nav1.5 current inactivation and slowed the recovery from Nav1.5 channel inactivation. The hesperetin-dependent blockage of Nav1.5 currents was frequency-dependent. Hesperetin also potently and reversibly inhibited Na + current (I Na ) in human atrial myocytes, consistently with its effects on Nav1.5 currents in HEK 293 cells. Conclusion: Hesperetin is a potent inhibitor of I Na in human atrial myocytes and Nav1.5 channels expressed in human embryonic kidney 293 cells. Hesperetin probably functions by blocking the open state and the inactivated state of these channels.

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Section: Introductionmentioning

confidence: 99%

Inhibitory effects of hesperetin on Nav1.5 channels stably expressed in HEK 293 cells and on the voltage-gated cardiac sodium current in human atrial myocytes

Wang

Zhang

et al. 2016

Acta Pharmacol Sin

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“…Citrus fruits are rich in flavanoids that have high antioxidant potential. Hesperetin, a dietary flavanoid, found in many citrus fruits is reported to possess ameliorative effect in diabetes induced vasculopathy via anti-angiogenic mechanism by inhibition in the expression of VEGF and PKC-β [105]. In another study106 these authors also reported the ameliorative effect of hesperetin in diabetic retinopathy via inhibiting retinal oxidative stress, neovascularisation as well as apoptosis in STZinduced diabetic rats.…”

Section: Role Of Antioxidants In Preventing Dvdmentioning

confidence: 93%

“…Recently, Kumar et al [104,105] investigated the retinoprotective properties of Moringa oleifera in STZ-diabetic rats. M. oleifera exhibit its retinoprotective effect via antioxidant, antiinflammatory, and anti-angiogenic mechanisms, which is attributed to its antioxidant constituents.…”

Section: Role Of Antioxidants In Preventing Dvdmentioning

confidence: 99%

An Insight in to the Pathogenesis of Diabetic Vascular Diseases: Role of Oxidative Stress and Antioxidants

Aditi¹,

Mahajan²,

Rawal³

et al. 2013

Pharm Anal Acta

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“…Coronary endothelial dysfunction occurs as a result of shift in the circulating EPCs 28 and DR may be attributed to a similar effect. Though STZ induced diabetic rat model is well established, 29,30 the timecourse of onset of DR in rat model varies in different studies and remains inconclusive. DR timeline is categorized into non-proliferative (leakage of vessels) and proliferative stage (proliferation of retinal vessels).…”

Section: Immunostaining Of Gfap In Retinamentioning

confidence: 99%

Differential Modulation of Circulating Endothelial Progenitor Cells in Peripheral Blood Monocyte Population of an Early Stage of Streptozotocin-Induced Diabetic Retinopathy

Muthaian¹,

Raveendran²

2016

JYP

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Male Wistar rats weighing 220-250 g were used for this study. The animals were individually acclimatized and fed a standard commercial diet and water ad libitum for 7 days. The 12 h light and 12 h dark cycle was followed throughout the study period. All the experiments and Retinal microvascular complications in STZ induced diabetic Wistar rats were validated after 4 months using trypsin digestion assay of retinal vasculature, histological analysis of retina, glial fibrillary acidic protein (GFAP) immunostaining. Subsequently, circulating EPCs were quantified in PBMCs from diabetes induced rats after 4 months using markers such as CD-34, CD-31, CD-146, VE-Cadherin and Flk-1 by flow cytometry. Results: Pericyte loss, acellular capillaries, retinal layer thickness, microglial activation and increased nitric oxide (NO) levels were observed after 4 months of diabetes induction. Whereas the EPC markers. While the EPC markers such as CD-34, CD-31, VE-Cadherin were decreased, the Flk-1+ve cells were up-regulated in the endogenous EPC pool. Conclusion: The quantity of EPCs is modulated in diabetes which may provide an insight into the use of EPCs as a biomarker for the progression of diabetes induced microvascular complication.

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Hesperetin rescues retinal oxidative stress, neuroinflammation and apoptosis in diabetic rats

Cited by 134 publications

References 44 publications

Inhibitory effects of hesperetin on Nav1.5 channels stably expressed in HEK 293 cells and on the voltage-gated cardiac sodium current in human atrial myocytes

Inhibitory effects of hesperetin on Nav1.5 channels stably expressed in HEK 293 cells and on the voltage-gated cardiac sodium current in human atrial myocytes

An Insight in to the Pathogenesis of Diabetic Vascular Diseases: Role of Oxidative Stress and Antioxidants

Differential Modulation of Circulating Endothelial Progenitor Cells in Peripheral Blood Monocyte Population of an Early Stage of Streptozotocin-Induced Diabetic Retinopathy

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