The neuroprotective effects of Tanshinone IIA are associated with induced nuclear translocation of TORC1 and upregulated expression of TORC1, pCREB and BDNF in the acute stage of ischemic stroke

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

“…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.…”

“…14) Researchers have reported that TSA can inhibit serum-withdrawal-and ethanol-induced apoptosis in cultured PC12 cells, and other studies have demonstrated that TSA has protective effects against focal cerebral I/R injury. 15) However, whether TSA has a neuroprotective effect against apoptosis remains unknown. Here, we studied the effects of TSA on cerebral apoptosis induced by middle cerebral artery occlusion (MCAO).…”

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

“…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]. Tang and coworkers [25] reported that the mRNA expression levels of Trx-1 and Trx-2 around the ischemia area were significantly increased (p < 0.05) in a brain transient ischemia model created by the blockage of the middle cerebral artery.…”

“…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.…”

Targeting ONOO^-/HMGB1/MMP-9 Signaling Cascades: Potential for Drug Development from Chinese Medicine to Attenuate Ischemic Brain Injury and Hemorrhagic Transformation Induced by Thrombolytic Treatment

“…The structure of tanshinone IIA is shown in figure 7. Tanshinone IIA demonstrated an antiapoptotic effect via upregulating blc-2 expression and downregulating active caspase-3 in the cortex, subsequently reducing neural apoptosis, decreasing the brain infarct volume and attenuating neurological deficit in a rat MCAO model [207,208]. In addition, tanshinone IIA scavenged RNS in an ischemic stroke model [209].…”