Tanshinone II A down-regulates HMGB1, RAGE, TLR4, NF-κB expression, ameliorates BBB permeability and endothelial cell function, and protects rat brains against focal ischemia

Wang, Lina; Zhang, Xiangjian; Liu, Lingling; Cui, Lili; Yang, Rui; Li, Min; Du, Wei

doi:10.1016/j.brainres.2009.12.046

Cited by 103 publications

(55 citation statements)

References 22 publications

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“…TSAII reduced the Aβ [25][26][27][28][29][30][31][32][33][34][35] -induced increase of caspase-3 activity and reduced the cytochrome C translocation into cytosol from mitochondria, protecting it from mitochondrial abnormalities [27]. In addition, TSIIA increased the expression of Bcl-2 in the ischemic cortex in TSIIA-treated ischemia groups and prevented an increase in the Bax/Bcl-2 ratio induced by neuronal damage [38].…”

Section: Tanshinone Iiamentioning

confidence: 90%

“…TSIIA can inhibit MIF expression, NF-κB activity, and the release of cytokines [42]. Wang and coworkers [22] substantiated the anti-inflammatory properties of TSAII in cerebral ischemia through the downregulation of HMGB1, the translocation from the nucleus to the cytoplasm of RAGE, TLR4, and NF-κB, and the upregulation claudin-5 expression. Moreover, exposure of cortical neurons to 30 µM Aβ [25][26][27][28][29][30][31][32][33][34][35] caused decreased activities of SOD and GSH-Px as well as increased levels of MDA production, while the pretreatment with TSAII attenuated the changes in SOD, GSH-Px, and MDA induced by the treatment of Aβ [25][26][27][28][29][30][31][32][33][34][35] [24].…”

Section: Tanshinone Iiamentioning

confidence: 96%

“…In all studies, cognitive impairment was improved and neurological deficits were reduced, suggesting that both tanshinones and despsides were able, even poorly, to pass the BBB and exert their therapeutical effect. Tanshinones, being lipophilic constituents, are administered orally [20] or intraperitoneally [21][22][23][24][25][26][27]. After 10-20 mg/kg, i. p. injections are effective in reducing infarct size, edema, and cell damage in models of cerebral ischemia.…”

Section: Effects Ofmentioning

confidence: 99%

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Effects of Salvia miltiorrhiza on CNS Neuronal Injury and Degeneration: A Plausible Complementary Role of Tanshinones and Depsides

Bonaccini

Karioti²,

Bergonzi

et al. 2015

Planta Med

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Section: Tanshinone Iiamentioning

confidence: 90%

Section: Tanshinone Iiamentioning

confidence: 96%

Section: Effects Ofmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Salvia miltiorrhiza on CNS Neuronal Injury and Degeneration: A Plausible Complementary Role of Tanshinones and Depsides

Bonaccini

Karioti²,

Bergonzi

et al. 2015

Planta Med

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“…Liu et al and Wang et al reported that, relative to the vehicle group, TSA (20 mg/kg) dramatically lessened neurological deficit scores, brain water content, and infarct sizes. 15,21) Tang et al showed that the TSA treatment could significantly attenuate the formation of brain edema and infarct area as determined 24 h after ischemic injury; 30 mg/ kg TSA was found to be most significant. 22) In the present study, we chose a concentration between 20 mg/kg and 30 mg/ kg and a markedly higher concentration 40 mg/kg.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Capabilities of Tanshinone IIA against Cerebral Ischemia/Reperfusion Injury via Anti-apoptotic Pathway in Rats

Chen

et al. 2012

Biological & Pharmaceutical Bulletin

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Danshen, derived from the dried root or rhizome of Salviae miltiorrhizae BGE., has Tanshinone IIA (TSA) as one of its active ingredients. Recent reports have shown that TSA can inhibit the apoptosis induced by serum withdrawal or ethanol in cultured PC12 cells. However, whether TSA has any neuroprotective effect remains unknown. In this study, we investigated the effects of TSA on cerebral apoptosis induced by middle cerebral artery occlusion (MCAO) in which cerebral ischemia had been induced 2 h earlier. Twenty-four hours after reperfusion, the rats were assessed for infarct volume etc. Intraperitoneal administration of 25 and 40 mg/kg TSA 10 min after MCAO significantly diminished infarct volume and brain water content and improved neurological deficits in a dose-dependent manner. The 25 mg/kg dosage was more effective. Treatment with 25 mg/kg TSA significantly improved symptoms and reduce infarct volume at different points in time, of which 10 min after MCAO was the most significant. Nissl-staining and HE-staining of the 25 mg/kg TSA group were more appreciable in terms of improvement relative to the vehicle group in the infarct core. TSA of dosage 25 mg/kg significantly decreased the expression of cleaved caspase-3 protein and increased the expression of B-cell lymphoma 2 (bcl-2) protein in the ischemic cortex. Fewer terminal deoxyribonucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick-end labeling (TUNEL)-positive cells were found in the penumbra of the treated group, but they were significantly more common in the vehicle group. We here conclude that the neuroprotective effects of TSA against focal cerebral ischemic/reperfusion injury are likely to be related to the attenuation of apoptosis.

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“…A recent report demonstrated that tanshinone IIA was effective for attenuating the extent of brain edema formation induced by cerebral ischemia injury in rats (13). Wang et al also reported that tanshinone IIA alleviated the brain damage caused by cerebral ischemia and the protective effect may be through the down-regulation of HMGB1, RAGE, TLR4 and NF-κB and the up-regulation of claudin-5 expression (14). It was also reported that Danshensu ameliorates the neurological deficit in cerebral ischemia/reperfusion rats (9).…”

Section: Discussionmentioning

confidence: 95%

Down-regulation of P-glycoprotein expression contributes to an increase in Danshensu accumulation in the cerebral ischemia/reperfusion brain

et al. 2011

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Abstract. P-glycoprotein (P-gp) plays a key role in the distribution and elimination of many clinically important therapeutic substances. P-gp inhibition is capable of increasing the concentration of various drugs in the brain. Danshensu is a main hydrophilic constituent of Salvia miltiorrhiza Bunge which is used traditionally to treat cerebrovascular diseases. In the present study, the effects of cerebral ischemia/reperfusion on the transport of Danshensu in the brain were observed by assaying the concentration at 15, 30 and 60 min after cerebral ischemia/reperfusion in the brain of rats. Furthermore, the expression of P-gp in the brain was also measured. Results showed that Danshensu concentrations in the ischemic hemisphere significantly increased compared to those in the non-ischemic hemisphere and the brain of the sham group. P-gp expression was inhibited by cerebral ischemia/reperfusion to some extent, and down-regulated much more by Danshensu treatment. The findings indicate that the down-regulation of P-gp expression induced by both cerebral ischemia/reperfusion and Danshensu treatment contributes to the increase of Danshensu accumulation in the brain.

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Tanshinone II A down-regulates HMGB1, RAGE, TLR4, NF-κB expression, ameliorates BBB permeability and endothelial cell function, and protects rat brains against focal ischemia

Cited by 103 publications

References 22 publications

Effects of Salvia miltiorrhiza on CNS Neuronal Injury and Degeneration: A Plausible Complementary Role of Tanshinones and Depsides

Effects of Salvia miltiorrhiza on CNS Neuronal Injury and Degeneration: A Plausible Complementary Role of Tanshinones and Depsides

Neuroprotective Capabilities of Tanshinone IIA against Cerebral Ischemia/Reperfusion Injury via Anti-apoptotic Pathway in Rats

Down-regulation of P-glycoprotein expression contributes to an increase in Danshensu accumulation in the cerebral ischemia/reperfusion brain

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