Protective effects of cationic bovine serum albumin-conjugated PEGylated tanshinone IIA nanoparticles on cerebral ischemia

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

“…This study showed that 15 µM Aβ [25][26][27][28][29][30][31][32][33][34][35] caused about 40 % additional LDH release from Aβ-treated cells compared with normal cells, and the cotreatment with SalB inhibited the LDH release from Aβ-treated cells. Lin and coworkers [53] investigated the neuroprotective effects of SalB on the expression of BPRP.…”

“…TSIIA decreased the expression of caspase-3 and caspase-8 and these results were proportional to the dose of TSIIA used [27]. 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].…”

“…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.…”

“…Shi and coworkers [40] elucidated the neuroprotective effects of TSAII against Aβ [25][26][27][28][29][30][31][32][33][34][35] -induced cytotoxicity and detected the association of this protective effect with calpain and the p35/Cdk5 pathway. TSAII increased the viability of neurons, decreased the expression of phosphorylated tau in neurons induced by Aβ [25][26][27][28][29][30][31][32][33][34][35] , maintained the normal expression of p35 on peripheral membranes, and decreased p25 expression in the cytoplasm. TanIIA also inhibited the translocation of Cdk5 from the nucleus into the cytoplasm of primary neurons induced by Aβ [25][26][27][28][29][30][31][32][33][34][35] .…”

“…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.…”