Tanshinone IIA prevents the loss of nigrostriatal dopaminergic neurons by inhibiting NADPH oxidase and iNOS in the MPTP model of Parkinson's disease

Ren, Bo; Zhang, Yuxin; Zhou, Hongxia; Sun, Fa-wei; Zhang, Zuo‐Feng; Wei, ZifFeng; Zhang, Chengyun; Si, Daowen

doi:10.1016/j.jns.2014.11.026

Cited by 62 publications

(40 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Here, we demonstrate that glutamate exposure increased Bax level, decreased Bcl-2 level, and promoted caspase-3 activation in SH-SY5Y cells and also found that tanshinone IIA was able to suppress these changes (Figure 4). This is in agreement with recent studies showing the inhibitory effect of tanshinone IIA on the cytotoxicity of several other neurotoxins, including the Parkinsonism-inducing 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 6-hydroxydopamine, through regulation of apoptosis-related protein expression [17, 54]. Together, these findings support the involvement of apoptosis pathways in the neuroprotective effects of tanshinone IIA.…”

Section: Discussionsupporting

confidence: 92%

“…The sulfonic sodium of tanshinone IIA is widely used to treat cardiovascular and cerebrovascular diseases [16]. Moreover, recent studies have shown that tanshinone IIA has beneficial effects on animal models of neurodegenerative disorders [17, 18]. For example, tanshinone IIA is capable of attenuating memory impairment in amyloid precursor protein/presenilin 1 transgenic mice via reducing accumulation of amyloid β -protein, a critical pathogenic protein in Alzheimer's disease, and activating synthesis of a synaptic brain-derived neurotrophic factor [18].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Tanshinone IIA Inhibits Glutamate‐Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH‐SY5Y Human Neuroblastoma Cells

Han

Wang

et al. 2017

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Glutamate excitotoxicity is associated with many neurological diseases, including cerebral ischemia and neurodegenerative diseases. Tanshinone IIA, a diterpenoid naphthoquinone from Salvia miltiorrhiza, has been shown to suppress presynaptic glutamate release, but its protective mechanism against glutamate-induced neurotoxicity is lacking. Using SH-SY5Y human neuroblastoma cells, we show here that excessive glutamate exposure decreases cell viability and proliferation and increases LDH release. Pretreatment with tanshinone IIA, however, prevents the decrease in cell viability and proliferation and the increase in LDH release induced by glutamate. Tanshinone IIA also attenuates glutamate-induced oxidative stress by reducing reactive oxygen species level and malondialdehyde and protein carbonyl contents and by enhancing activities and protein levels of superoxide dismutase and catalase. We then show that tanshinone IIA prevents glutamate-induced mitochondrial dysfunction by increasing mitochondrial membrane potential and ATP content and by reducing mitochondrial protein carbonyl content. Moreover, tanshinone IIA can inhibit glutamate-induced apoptosis through regulation of apoptosis-related protein expression and MAPK activation, including elevation of Bcl-2 protein level, decrease in Bax and cleaved caspase-3 levels, and suppression of JNK and p38 MAPK activation. Collectively, our findings demonstrate that tanshinone IIA protects SH-SY5Y cells against glutamate toxicity by reducing oxidative stress and regulating apoptosis and MAPK pathways.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA Inhibits Glutamate‐Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH‐SY5Y Human Neuroblastoma Cells

Han

Wang

et al. 2017

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…At an advanced stage of CIRI, NO generated by iNOS can intensify the toxicity of glutamic acid and result in delayed neuronal damage (27). Particularly, the close integration of iNOS and calmodulin further aggravates DND (30,31). In this study, we found that SIRT1 exerted neuroprotective effects by suppressing iNOS protein expression in rats with CIRI.…”

Section: Discussionmentioning

confidence: 57%

SIRT1 exerts neuroprotective effects by attenuating cerebral ischemia/reperfusion-induced injury via targeting p53/microRNA-22

Wang

2016

International Journal of Molecular Medicine

View full text Add to dashboard Cite

Abstract. The aim of this study was to investigate whether the SIRT1 exerts neuroprotective effects by attenuating cerebral ischemia/reperfusion-induced injury (CIRI) via targeting p53/microRNA-22. We found that the overexpression of sirtuin 1 (SIRT1) decreased the infarct volume, suppressed p53 protein expression and activated microRNA-22 expression following CIRI. An injection of lipopolysaccharide (LPS, 1 mg/ml; Sigma, St. Louis, MO USA) into the corpus callosum was used to induce CIRI in rats. The infarct volume and neurological deficit score were used to examine the effects of SIRT1 on CIRI. Furthermore, the overexpression of SIRT1 was found to suppress caspase-3 activity, inhibit the activation of the Bax signaling pathway, reduce tumor necrosis factor-α (TNF-α) and interleukin (IL)-6) activity, decrease cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) protein expression, and increase IL-10 activity following CIRI. Following the downregulation of SIRT1, p53 protein expression was significantly increased, microRNA-22 expression was inhibited, caspase-3 activity was increased and the Bax signaling pathway was activated. In addition, the activity of TNF-α and IL-6 was was enhanced, COX-2 and iNOS protein expression was increased, and IL-10 activity was reduced following CIRI. Thus, the data from our study suggest that SIRT1 attenuates CIRI by targeting the p53/microRNA-22 axix, while suppressing apoptosis, inflammation, COX-2 and iNOS expression.

show abstract

“…If confirmed, these findings might suggest a connection between seizures and peripheral inflammation and provide an additional rationale for the use of antiepileptic botanical extract or compounds, which also exhibit antiinflammatory activity. It is beyond the scope of our paper to review the extensive and rapidly growing literature on antiinflammatory effects of botanicals in microglia, but some of the compounds of interest in the context of this paper include, for example, baicalin, curcumin, resveratrol, tanshinone IIA, wogonin, and ursolic acid, among many others [205][206][207][208][209][210][211][212][213]. Baicalin and wogonin have also been shown to exhibit a plethora of other pharmacological effects.…”

Section: What Does It All Mean?mentioning

confidence: 99%

A pharmacological basis of herbal medicines for epilepsy

Sucher¹,

Carles²

2015

Epilepsy & Behavior

125

View full text Add to dashboard Cite

Tanshinone IIA prevents the loss of nigrostriatal dopaminergic neurons by inhibiting NADPH oxidase and iNOS in the MPTP model of Parkinson's disease

Cited by 62 publications

References 36 publications

Tanshinone IIA Inhibits Glutamate‐Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH‐SY5Y Human Neuroblastoma Cells

Tanshinone IIA Inhibits Glutamate‐Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH‐SY5Y Human Neuroblastoma Cells

SIRT1 exerts neuroprotective effects by attenuating cerebral ischemia/reperfusion-induced injury via targeting p53/microRNA-22

A pharmacological basis of herbal medicines for epilepsy

Contact Info

Product

Resources

About