Apoptosis induced neurotoxicity of Di-n-butyl-di-(4-chlorobenzohydroxamato) Tin (IV) via mitochondria-mediated pathway in PC12 cells

Ge, Rui; Ma, Wen-Hua; Li, Yunlan; Liu, Qingshan

doi:10.1016/j.tiv.2012.08.009

Cited by 25 publications

(20 citation statements)

References 26 publications

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“…Cell viability was examined by MTT assay evidence, including oxidative stress, has established a link between various disturbances in mitochondrial functioning and diabetic neuropathy [1][2][3][4]. In the present study, DSePA pretreatment observably alleviated high glucose-induced disruption of Δψm, which is consistent with the hypothesis that the loss of Δψm as an early cellular event in response to apoptotic stimuli plays a key role in launching the mitochondria-mediated apoptosis pathway [43]. Bcl-2 family can affect and regulate the mitochondrial permeability and play critical roles in modulating mitochondria-mediated apoptosis [44,45].…”

Section: Discussionsupporting

confidence: 89%

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

Wang

et al. 2015

Mol Neurobiol

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Hyperglycemia as the major hallmark of diabetic neuropathy severely limited its therapeutic efficiency. Evidences have revealed that selenium (Se) as an essential trace element could effectively reduce the risk of neurological diseases. In the present study, 3,3'-diselenodipropionic acid (DSePA), a derivative of selenocystine, was employed to investigate its protective effect against high glucose-induced neurotoxicity in PC12 cells and evaluate the underlying mechanism. The results suggested that high glucose showed significant cytotoxicity through launching mitochondria-mediated apoptosis in PC12 cells, accompanied by poly (ADP-ribose) polymerase (PARP) cleavage, caspase activation, and mitochondrial dysfunction. Moreover, high glucose also triggered DNA damage and dysregulation of MAPKs and AKT pathways through reactive oxygen species (ROS) overproduction. p53 RNA interference partially suppressed high glucose-induced cytotoxicity and apoptosis, indicating the role of p53 in high glucose-induced signal. However, DSePA pretreatment effectively attenuated high glucose-induced cytotoxicity, inhibited the mitochondrial dysfunction through regulation of Bcl-2 family, and ultimately reversed high glucose-induced apoptotic cell death in PC12 cells. Attenuation of caspase activation, PARP cleavage, DNA damage, and ROS accumulation all confirmed its protective effects. Moreover, DSePA markedly alleviated the dysregulation of AKT and MAPKs pathways induced by high glucose. Our findings revealed that the strategy of using DSePA to antagonize high glucose-induced neurotoxicity may be a highly effective strategy in combating high glucose-mediated neurological diseases.

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Section: Discussionsupporting

confidence: 89%

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

Wang

et al. 2015

Mol Neurobiol

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“…7) Besides, p38 activation has been implicated in modulating apoptosis in PC12 and rat cerebellar granule cells. 8,9) A recent study also supported the fact that p38 was activated in neonatal rat cardiomyocytes subjected to ischemia and that inhibition of p38 evidently protected cardiac myocytes from apoptosis. 10) In the meantime, Wang et al 11) found that specific activation of JNK pathway through transfecting cultured rat neonatal cardiomyocytes with MKK7, an upstream activator of JNK, led to induction of hypertrophic responses rather than apoptosis.…”

mentioning

confidence: 75%

Baicalin Attenuates Acute Myocardial Infarction of Rats <i>via</i> Mediating the Mitogen-Activated Protein Kinase Pathway

Liu

Fan

Shi

et al. 2013

Biological & Pharmaceutical Bulletin

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Baicalin is a bioactive ingredient from the herb and has possessed various pharmacological actions. The present study was performed to evaluate the cardioprotective potential of baicalin against myocardial infarction and explore the potential mechanism. Baicalin was intraperitoneally injected into the rats by the doses of 50, 100 and 200 mg/kg, respectively, once a day for 7 d and, 30 min after the last administration, the left coronary artery was ligated. Infarct size was measured to analyze the myocardial damage. Myocardial specific enzymes, including creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) were determined with the colorimetric method. Evidence for myocardial apoptosis was detected by caspase-3 activity measurement and Western blot analysis. We also examined the protein levels of three major subgroups of mitogen-activated protein kinases (MAPKs), namely, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 by immuoblotting. Our results indicated that baicalin significantly reduced the infarct size and myocardial enzymes (CK, CK-MB, LDH and cTnT). Administration of baicalin also suppressed the activity and protein expression of caspase-3. Moreover, the protein level of phosphorylated ERK (p-ERK) was found to be evidently augmented while the phosphorylated JNK (p-JNK) and phosphorylated p38 (p-p38) were strikingly diminished in infarcted rats with baicalin treatment. These findings suggest that the baicalin's cardioprotection associates with mediation of MAPK cascades in acute myocardial infarction of rats.

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“…The opening of this pore is accompanied by membrane potential (ΔΨ) collapse, calcium release, uptake of electrolytes and water, matrix swelling and ruptures of the mitochondrial outer membrane [42] . As a consequence, several factors are released into the cytosol including cytochrome c, apoptotic peptidase activating factor 1 (apaf-1), apoptosis-inducing factor (AIF) and caspase family members, which participate in apoptosis pathways [43][44][45] . Several agents, such as Ca 2+ , thiol oxidants, reactive oxygen species (ROS), and/or members of the Bcl -2 family of proteins can regulate cell death or survival by interference with MPTP opening [46][47][48] .…”

Section: Discussionmentioning

confidence: 99%

African eggplant (Solanum anguivi Lam.) fruit with bioactive polyphenolic compounds exerts in vitro antioxidant properties and inhibits Ca2+-induced mitochondrial swelling

Elekofehinti

Kamdem

Bolingon

et al. 2013

Asian Pacific Journal of Tropical Biomedicine

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Apoptosis induced neurotoxicity of Di-n-butyl-di-(4-chlorobenzohydroxamato) Tin (IV) via mitochondria-mediated pathway in PC12 cells

Cited by 25 publications

References 26 publications

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

Baicalin Attenuates Acute Myocardial Infarction of Rats <i>via</i> Mediating the Mitogen-Activated Protein Kinase Pathway

African eggplant (Solanum anguivi Lam.) fruit with bioactive polyphenolic compounds exerts in vitro antioxidant properties and inhibits Ca2+-induced mitochondrial swelling

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