Ginsenoside Rd attenuates early oxidative damage and sequential inflammatory response after transient focal ischemia in rats

Introduction: This study aimed to investigate whether epigallocatechin-3-gallate (EGCG) shows antioxidant activity against angiotensin II (Ang II)-induced human umbilical vein endothelial cell (HUVEC) apoptosis. Materials and Methods: The viability of HUVECs was revealed by MTT and LDH assay. The cell apoptosis was detected by FITC-PI assay. A fluorescent probe assay was used to measure the reactive oxygen species (ROS) generation in HUVECs. Mitochondrial permeability transition pore (MPTP) opening, mitochondrial membrane potential, and caspase-3, -4, -8, -9 activities were also measured. Results: We found that Ang II treatment increased the generation of ROS, enhanced MPTP opening and cytochrome c release, activated caspase-3/9, and consequently induced HUVEC apoptosis. EGCG treatment-suppressed Ang II induces the oxidative stress of HUVECs and mitochondria-related cell apoptosis. We also showed that the antioxidant activity pathway, including cytochrome c release, MPTP opening, and caspase-3/9 activation, is a key endogenous defensive system in HUVECs, provoking Ang II exposure. Our study revealed that increased expression of Nrf2 by EGCG could partially repress Ang II-induced injury effects. Conclusions: All of our findings indicated that EGCG treatment provides a protective effect for Ang II-induced HUVEC apoptosis by decreasing oxidative stress and ameliorating mitochondrial injury.

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“…Protein carbonyl concentrations were calculated using an ELISA kit (Cell Biolabs, USA) [23]. All standards and samples were run in duplicate.…”

Section: Methodsmentioning

confidence: 99%

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

et al. 2017

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“…Protein carbonyl content was assayed as we previously described [18] using a commercial ELISA kit (Cell Biolabs, USA). All standards and samples were run in duplicate.…”

Section: Measurement Of Oxidative Productsmentioning

confidence: 99%

Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics

Liu

Mao

Wang

et al. 2015

Cell Physiol Biochem

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Background: Parkinson disease (PD) is a common adult-onset neurodegenerative disorder, and PD related neuronal injury is associated with oxidative stress and mitochondrial dysfunction. Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies. Methods: The present study aimed to investigate the potential protective role of allicin in an in vitro PD model induced by 6-hydroxydopamine (6-OHDA) in PC12 cells. The protective effects were measured by cell viability, decreased lactate dehydrogenase (LDH) release and flow cytometry, and the anti-oxidative activity was determined by reactive oxygen species (ROS) generation, lipid peroxidation and the endogenous antioxidant enzyme activities. Mitochondrial function in PC12 cells was detected by mitochondrial membrane potential (MMP) collapse, cytochrome c release, mitochondrial ATP synthesis, and the mitochondrial Ca²⁺ buffering capacity. To investigate the potential mechanism, we also measured the expression of mitochondrial biogenesis factors, mitochondrial morphological dynamic changes, as well as detected mitochondrial dynamic proteins by western blot. Results: We found that allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure. Allicin also inhibited ROS generation, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities. These protective effects were associated with suppressed mitochondrial dysfunction, as evidenced by decreased MMP collapse and cytochrome c release, preserved mitochondrial ATP synthesis, and the promotion of mitochondrial Ca²⁺ buffering capacity. In addition, allicin significantly enhanced mitochondrial biogenesis and prevented fragmentation of mitochondrial network after 6-OHDA treatment. The results of western blot analysis showed that the 6-OHDA induced decrease in the expression of optic atrophy type 1 (Opa-1), increase in mitochondrial fission 1 (Fis-1) and dynamin-related protein 1 (Drp-1) were all partially revised by allicin. Conclusion: In summary, our data strongly suggested that allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.

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“…We have previously reported that Rd protects against neuronal oxidative damage induced by hydrogen peroxide [5] and oxygen-glucose deprivation [6]. More recently, we suggested that Rd exerts neuroprotection against transient focal ischemia in an integrated process of free radicals scavenging, mitochondrial protection, energy restoration, and apoptosis inhibition [7,8]. Alternatively, in a model of excitotoxicity, Rd attenuates the Ca 2+ overload and apoptosis produced by exposure of neuronal cultures to glutamate [28].…”

Section: Discussionmentioning

confidence: 99%

“…Previously, we found that Rd could protect against neuronal oxidative damage induced by hydrogen peroxide [5] and oxygen-glucose deprivation [6], an in vitro model of cerebral ischemia. More recently, Rd was reported to ameliorate histological and functional outcome after focal cerebral ischemia [7][8][9], which is associated with mitochondrial protection and energy restoration. However, the preclinical characteristics of the neuroprotective effects of Rd have not been fully defined.…”

Section: (S)-triol-(20-o-b-d-glucopyranosyl)-3-o-b-d-glucopyranosyl-(mentioning

confidence: 99%

Ginsenoside Rd in Experimental Stroke: Superior Neuroprotective Efficacy with a Wide Therapeutic Window

Kong

Yang

et al. 2011

Neurotherapeutics

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Ginsenoside Rd (Rd), one of the main active ingredients in Panax ginseng, has been demonstrated to protect against ischemic cerebral damage in vitro and in vivo. In this study, we aimed to further define the preclinical characteristics of Rd. We show that Rd passes the intact blood-brain barrier and exerts protection in both transient and permanent middle cerebral artery occlusion (MCAO) in rats. In the dose-response study, Rd (10-50 mg/Kg) significantly reduced the infarct volume on postoperative days (PODs) 1, 3, and 7. This protection was associated with an improved neurological outcome for as many as 6 weeks after transient MCAO, as assessed by modified neurological severity score, modified sticky-tape test, and corner test. For comparison, Rd was significantly more effective than edaravone and slightly more effective than Ntert-butyl-alpha-phenylnitrone (PBN). In the therapeutic window study, Rd exhibited remarkable neuroprotection, even when administered for as many as 4 h after the recirculation of transient MCAO or after the onset of permanent MCAO. Furthermore, in female rats or 16-month-old male rats, the salutary effects of Rd were also observed. These findings suggest Rd is a promising neuroprotectant and provide support for future clinical studies to confirm whether Rd is beneficial in ischemic stroke.

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Ginsenoside Rd attenuates early oxidative damage and sequential inflammatory response after transient focal ischemia in rats

Cited by 124 publications

References 34 publications

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics

Ginsenoside Rd in Experimental Stroke: Superior Neuroprotective Efficacy with a Wide Therapeutic Window

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