Inhibition by epigallocatechin gallate of CoCl2-induced apoptosis in rat PC12 cells

Jung, Ji‐Yeon; Mo, Hyun-Chul; Yang, Keun–Hyeok; Jeong, Yoseok; Yoo, Hyeon-Gyeong; Choi, Nam-Ki; Oh, Won-Mann; Oh, Hee-Kyun; Kim, Sun-Hun; Lee, Jin Ha; Kim, Hyun‐Jin; Kim, Wonjae

doi:10.1016/j.lfs.2006.11.033

Cited by 66 publications

(47 citation statements)

References 36 publications

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“…27 Importantly, chloroplasts not only provide cell with the energy but also represent a sensor of environmental information, and chloroplast redox signals help to acclimate the organism to environmental stresses. 28 In the present paper, NaCl -induced K C efflux in leaf mesophyll was investigated in samples pre-treated with methyl viologen (MV, a redox-active compound that generates superoxide anions in chloroplasts), 29 32,33 It is widely used in animal research, [34][35][36][37] and was also applied to plant species by several authors. 38,39 As showed in Figure 2, specimens pre-treated with MV showed significantly higher NaCl -induced peak K C efflux from leaf mesophyll as compared with non-treated control.…”

Section: Naclmentioning

confidence: 99%

Chloroplast-generated ROS dominate NaCl^-induced K⁺efflux in wheat leaf mesophyll

Shabala

Zhou

et al. 2015

Plant Signaling & Behavior

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Section: Naclmentioning

confidence: 99%

Chloroplast-generated ROS dominate NaCl^-induced K⁺efflux in wheat leaf mesophyll

Shabala

Zhou

et al. 2015

Plant Signaling & Behavior

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“…Numerous studies have demonstrated that cobalt chloride (CoCl 2 ), as a chemical hypoxia agent, can mimic the hypoxic/ ischemic condition and induce the generation of ROS and cytotoxicity (Chen et al, 2010;Jung and Kim, 2004;Jung et al, 2007;Zou et al, 2001). Accumulating evidence showed that CoCl 2 exposure induced inflammatory response, characterized by enhanced secretion of interleukin-6 (IL-6) and interleukin-8 (IL-8) in endotheliocyte and astrocytes (Kim et al, 2006;Montopoli et al, 2007;Schmalz et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

Liu

Ling

Mei-fen

et al. 2011

Molecules and Cells

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Hypoxia of skin is an important physiopathological process in many diseases, such as pressure ulcer, diabetic ulcer, and varicose ulcer. Although cellular injury and inflammation have been involved in hypoxia-induced dermatic injury, the underlying mechanisms remain largely unknown. This study was conducted to investigate the effects of cobalt chloride (CoCl 2 ), a hypoxia-mimicking agent, on human skin keratinocytes (HaCaT cells) and to explore the possible molecular mechanisms. Exposure of HaCaT cells to CoCl 2 reduced cell viability and caused overproduction of reactive oxygen species (ROS) and oversecretion of interleukin-6 (IL-6) and interleukin-8 (IL-8). Importantly, CoCl 2 exposure elicited overexpression of cyclooxygenase-2 (COX-2) and phosphorylation of nuclear factor-kappa B (NF-κB) p65 subunit. Inhibition of COX-2 by NS-398, a selective inhibitor of COX-2, significantly repressed the cytotoxicity, as well as secretion of IL-6 and IL-8 induced by CoCl 2 . Inhibition of NF-κB by PDTC (a selective inhibitor of NF-κB) or genetic silencing of p65 by RNAi (Si-p65), attenuated not only the cytotoxicity and secretion of IL-6 and IL-8, but also overexpression of COX-2 in CoCl 2 -treated HaCaT cells. Neutralizing anti-IL-6 or anti-IL-8 antibody statistically alleviated CoCl 2 -induced cytotoxicity in HaCaT cells. N-acetyl-L-cysteine (NAC), a well characterized ROS scavenger, obviously suppressed CoCl 2 -induced cytotoxicity in HaCaT cells, as well as secretion of IL-6 and IL-8. Additionally, NAC also repressed overexpression of COX-2 and phosphorylation of NF-B κ p65 subunit induced by CoCl 2 in HaCaT cells. In conclusion, our results demonstrated that oxidative stress mediates chemical hypoxia-induced injury and inflammatory response through activation of NF-κB-COX-2 pathway in HaCaT cells.

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“…9,10) In this study, we find that PC12 cells provide a useful in vitro system for the study of hypoxia-induced neuronal injury upon exposure to CoCl 2 . 11,12) Salidroside (SA), a natural compound from Rhodiola rosea L., is a major active ingredient responsible for most pharmacological effects of Rhodiola, such as anti-oxidative, anti-aging, anti-inflammatory, anti-cancer, anti-fatigue and anti-depressant activities. [13][14][15][16][17][18][19] Increasing evidence suggests that SA may have neuroprotective effects in injured brain.…”

mentioning

confidence: 99%

Effects of <i>Salidroside</i> on Cobalt Chloride-Induced Hypoxia Damage and mTOR Signaling Repression in PC12 Cells

Zhong

Lin

et al. 2014

Biological & Pharmaceutical Bulletin

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Salidroside (SA), a phenylpropanoid glycoside isolated from Rhodiola rosea L., has been documented to exert a broad spectrum of pharmacological properties, including protective effects against neuronal death induced by various stresses. To provide further insights into the neuroprotective functions of SA, this study examined whether SA can attenuate cobalt chloride (CoCl 2 )-induced hypoxia damage and mammalian target of rapamycin (mTOR) signaling repression in PC12 differentiated cells. Differentiated PC12 cells were exposed to CoCl 2 for 12 h to mimic hypoxic/ischemic conditions and treated with SA at the same time, followed by electron microscopy and analysis of cell viability, intracellular reactive oxygen species ( Key words salidroside; ischemic; mammalian target of rapamycin (mTOR); hypoxia; cobalt chloride; PC12 cell Focal cerebral ischemia or stroke is characterized by obstruction of blood flow to the brain, resulting in deficient supply of oxygen, glucose, serum, and nutrient that are indispensable for the energy generation. Since central nervous system is most susceptible to hypoxia conditions, the continuous oxygen and energy deprivation results in cognitive disturbances and decreased motor control, leading to fainting, long term loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death. Ischemic stroke is currently a leading cause of disability and mortality in the aged population, due to limited medication and therapy, and new therapeutic strategies for this devastating disease are urgently needed.Recently, the role of mammalian target of rapamycin (mTOR) signaling in neurodegenerative and cerebrovascular diseases has attracted great attention.

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Inhibition by epigallocatechin gallate of CoCl2-induced apoptosis in rat PC12 cells

Cited by 66 publications

References 36 publications

Chloroplast-generated ROS dominate NaCl^-induced K⁺efflux in wheat leaf mesophyll

Chloroplast-generated ROS dominate NaCl^-induced K⁺efflux in wheat leaf mesophyll

Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

Effects of <i>Salidroside</i> on Cobalt Chloride-Induced Hypoxia Damage and mTOR Signaling Repression in PC12 Cells

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Inhibition by epigallocatechin gallate of CoCl2-induced apoptosis in rat PC12 cells

Cited by 66 publications

References 36 publications

Chloroplast-generated ROS dominate NaCl-induced K+efflux in wheat leaf mesophyll

Chloroplast-generated ROS dominate NaCl-induced K+efflux in wheat leaf mesophyll

Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

Effects of <i>Salidroside</i> on Cobalt Chloride-Induced Hypoxia Damage and mTOR Signaling Repression in PC12 Cells

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Chloroplast-generated ROS dominate NaCl^-induced K⁺efflux in wheat leaf mesophyll

Chloroplast-generated ROS dominate NaCl^-induced K⁺efflux in wheat leaf mesophyll