Protective Effects of Salidroside on Endothelial Cell Apoptosis Induced by Cobalt Chloride

Tan, Chu-Bing; Gao, Mei Hua; Xu, Weifeng; Yang, Xiuying; Zhu, Xiaoming; Du, Guanhua

doi:10.1248/bpb.32.1359

Cited by 60 publications

(38 citation statements)

References 23 publications

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“…The increased formation of ROS is thought to be a key event in the pathogenesis of DR. 17) On the other hand, it is known that both hypoxia and hypoxia-mimicking agents increase ROS generation and activation of several intracellular signaling pathways. 10,18) In this study, CoCl 2 decreased the expression of EC-SOD accompanied with the increase of VEGF, a pro-inflammatory factor. Pre-treatment with NAC significantly suppressed the ROS production, down-regulation of EC-SOD, and up-regulation of VEGF induced by CoCl 2 .…”

Section: Discussionsupporting

confidence: 50%

Effect of Hypoxia Mimetic Cobalt Chloride on the Expression of Extracellular-Superoxide Dismutase in Retinal Pericytes

Adachi

Aida

Nishihara

et al. 2011

Biological & Pharmaceutical Bulletin

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The initial clinical stage of diabetic retinopathy (DR) is characterized by the development of intraretinal microvascular abnormalities. The increased formation of reactive oxygen species (ROS) is thought to be a key event in the pathogenesis of DR. Extracellular-superoxide dismutase (EC-SOD) is an anti-inflammatory enzyme that is distributed mainly in vascular cells and protects cells from ROS by scavenging superoxide anion. Treatment with cobalt chloride (CoCl 2 ) decreased the expression of EC-SOD but not other SOD isozymes in pericytes accompanied with an increase of intracellular ROS production. Pre-treatment with N-acetylcysteine (NAC) significantly suppressed the ROS production and down-regulation of EC-SOD. We observed the activation of caspase-3 and DNA fragmentation as signs of apoptotic process by CoCl 2 treatment. In addition, these phenomena were significantly inhibited by pre-treatment with NAC. EC-SOD enhancer 4-phenyl butyric acid also suppressed the caspase-3 activation. It is known that the presence of a high level of EC-SOD throughout the vessel walls might have an important protective role against superoxide in the vascular system. The decrease in EC-SOD expression accompanied with elevation of ROS level in pericytes under hypoxia might induce and/or promote the ROStriggered apoptosis of pericytes and the development of pathogenesis in DR.

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Section: Discussionsupporting

confidence: 50%

Effect of Hypoxia Mimetic Cobalt Chloride on the Expression of Extracellular-Superoxide Dismutase in Retinal Pericytes

Adachi

Aida

Nishihara

et al. 2011

Biological & Pharmaceutical Bulletin

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“…Unfortunately, the mechanisms underlying these changes have not been clearly delineated, and no suitable drug that can reverse these changes has been identified. According to a research conducted by Tan et al [26], SAL may represent a novel therapeutic agent for the treatment and prevention of hypoxia and oxidative stress-related diseases via targeting HIF-1α, indicating the possible target of SAL in FSGS. HIF-1α is activated under hypoxia and promotes expression of genes involved in cell fate, angiogenesis, and glucose metabolism [11,12].…”

Section: Discussionmentioning

confidence: 99%

Salidroside Attenuates Adriamycin-Induced Focal Segmental Glomerulosclerosis by Inhibiting the Hypoxia-Inducible Factor-1α Expression Through Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway

Liu¹,

2019

Nephron

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Background: Focal segmental glomerulosclerosis (FSGS) is a common histologic pattern of kidney injury, which may eventually lead to end-stage renal disease. Objectives: Salidroside (SAL, p-hydroxyphenyl-β-D-glucoside) is an active component isolated from Rhodiolarosea, which has various pharmacological properties including anti-inflammation and antioxidation. SAL may attenuate FSGS, but the underlying mechanism is not clear. Thus, in this study, we focus on the renoprotective role of SAL in FSGS using Adriamycin nephropathy (AN) mouse models. Methods: In C57 BL/6 mice, AN was induced by Adriamycin (10 mg/kg body weight, diluted in normal saline) via a tail vein on day 0. Then they were organized into 6 groups for the animal experiments: AN + saline group; AN + SAL group (40 mg/kg); AN + LY294002 (a selective phosphatidylinositol 3-kinase [PI3K] inhibitors, 50 mg/kg) group; AN + SAL + LY294002 group; AN + YC-1 (a selective hypoxia-inducible factor-1α [HIF-1α] inhibitors, 50 mg/kg) group; and AN + SAL + YC-1 group. All of the drugs were given on the day of Adriamycin injection and continued for 6 weeks, and the drugs were given by intraperitoneally. At 6 weeks, the mice were sacrificed; kidneys and blood samples were collected for further analysis. Results: In FSGS mouse models, SAL treatment could ameliorate proteinuria, renal function, and markers of Nephrotic Syndrome inhibit alpha-smooth muscle actin and fibronectin expression and downregulates the expression of HIF-1α. Besides, the levels of PI3K and p-protein kinase B (Akt) in renal tissues were significantly decreased after SAL injection. Eventually, SAL treatment results reduced inflammatory cytokines and reactive oxygen species production. Conclusions: In summary, SAL ameliorates FSGS mainly by inhibiting the expression of HIF-1α through PI3K/Akt pathway, which might offer an array of hope for ameliorating FSGS.

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“…1a), has been documented to possess neuroprotective effects against neuronal damage induced by various insults. [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33] However, the underlying mechanisms are still not well understood.…”

Section: Discussionmentioning

confidence: 99%

“…SA can reduce the degree of cerebral edema and the brain infarct size of rats with global cerebral ischemia, relieve the metabolism abnormity of free radicals and improve the function of cognition as well as behavioral and histological outcomes. [20][21][22] [23][24][25][26][27][28][29][30][31][32][33] In addition, it has been reported that SA may regulate mTOR signaling in cultured human umbilical vein endothelial cells (HUVECs) or in bladder cancer cell lines. 34,35) However, whether the neuroprotective effects of SA involve regulation of the mTOR signaling pathway in PC12 cells is still unknown.…”

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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Protective Effects of Salidroside on Endothelial Cell Apoptosis Induced by Cobalt Chloride

Cited by 60 publications

References 23 publications

Effect of Hypoxia Mimetic Cobalt Chloride on the Expression of Extracellular-Superoxide Dismutase in Retinal Pericytes

Effect of Hypoxia Mimetic Cobalt Chloride on the Expression of Extracellular-Superoxide Dismutase in Retinal Pericytes

Salidroside Attenuates Adriamycin-Induced Focal Segmental Glomerulosclerosis by Inhibiting the Hypoxia-Inducible Factor-1α Expression Through Phosphatidylinositol 3-Kinase/Protein Kinase B Pathway

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

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