“…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].…”
Section: Tanshinone Iiamentioning
confidence: 86%
“…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] . Fan and coworkers [41] demonstrated that TSAII exerts anti-inflammatory effects by inhibition of inflammation cytokine (IL-1β, IL-6, and TNF-α) expression via the ER-dependent pathway and inhibition of iNOS gene expression and NO production.…”
Section: Tanshinone Iiamentioning
confidence: 95%
“…The nanoparticles effectively reduced infarction volume, neurological dysfunctions, neutrophils infiltration, and neuronal apoptosis. Similar models of CNS trauma have been investigated with hydrophilic depsides, which are administered intravenously [28][29][30] or orally [31][32][33][34]. Similar doses were used by i. v. administration or per os (10-60 mg/kg), with all the cases having positive outcomes and, also, lower dosages.…”
Section: Effects Ofmentioning
confidence: 99%
“…From the above results, the fact that such different compounds having remarkable different structures, sizes, and polarity can act in the same way in CNS neuronal injury and degeneration it is quite extraordinary. Additionally, it is noteworthy that SalB [30,[32][33][34], a tetramer of caffeic acid, caffeic acid dimer [29], and the smaller analog danshensu (3,4-dihydroxyphenyllactic acid) [28,31] …”
Section: Effects Ofmentioning
confidence: 99%
“…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] .…”
Salvia miltiorrhiza l " Lamiaceae l " tanshinones and depsides l " CNS neuronal injury and degeneration l " in vivo studies l " biochemical mechanisms l " pharmacokinetics
“…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].…”
Section: Tanshinone Iiamentioning
confidence: 86%
“…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] . Fan and coworkers [41] demonstrated that TSAII exerts anti-inflammatory effects by inhibition of inflammation cytokine (IL-1β, IL-6, and TNF-α) expression via the ER-dependent pathway and inhibition of iNOS gene expression and NO production.…”
Section: Tanshinone Iiamentioning
confidence: 95%
“…The nanoparticles effectively reduced infarction volume, neurological dysfunctions, neutrophils infiltration, and neuronal apoptosis. Similar models of CNS trauma have been investigated with hydrophilic depsides, which are administered intravenously [28][29][30] or orally [31][32][33][34]. Similar doses were used by i. v. administration or per os (10-60 mg/kg), with all the cases having positive outcomes and, also, lower dosages.…”
Section: Effects Ofmentioning
confidence: 99%
“…From the above results, the fact that such different compounds having remarkable different structures, sizes, and polarity can act in the same way in CNS neuronal injury and degeneration it is quite extraordinary. Additionally, it is noteworthy that SalB [30,[32][33][34], a tetramer of caffeic acid, caffeic acid dimer [29], and the smaller analog danshensu (3,4-dihydroxyphenyllactic acid) [28,31] …”
Section: Effects Ofmentioning
confidence: 99%
“…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] .…”
Salvia miltiorrhiza l " Lamiaceae l " tanshinones and depsides l " CNS neuronal injury and degeneration l " in vivo studies l " biochemical mechanisms l " pharmacokinetics
Recent studies have shown that block wnt/ b-catenin signaling pathway is integrant for cardiomyocytes differentiation from bone marrow mesenchymal stem cells (MSCs). By transducing the MSCs with lentivirus which contain b-catenin interference RNA, we screened out the non b-catenin expression clone. In the establishment of knockdown b-catenin in MSCs, we investigated the role of 5-azacytidine (5-aza), salvianolic acid B (salB), and cardiomyocytes lysis medium (CLM) in inducing MSCs to differentiate into cardiomyocyte-like cells. A method for culturing MSCs and cardiomyocytes was established. Purified MSCs were investigated by flow cytometry. The MSCs were positive for CD90 and CD29, but negative for CD34 and CD45. Meanwhile, the cardiomyocytes contracted spontaneously after 24 h of seeding into the plates. The fourth-passage non-b-catenin expression MSCs were divided into eight groups: control group, 5-aza, salB, CLM, 5-aza ? salB, 5-aza ? CLM, salB ? CLM, and 5-aza ? salB ? CLM. The gene and protein expression of cTnT, a-actin, b-myosin, b-catenin, and GSK-3b were detected by quantitative real-time PCR and Western blotting. Our results showed that cTnT expression in 5-aza ? salB ? CLM group was ninefold higher than in the control group in the non-b-catenin MSCs model, implying that cardiomyocytes differentiation from MSCs is an extremely complicated process and it is necessary to consider the internal and external environmental conditions, such as suitable pharmaceutical inducers, cardiomyocytes microenvironments, inhibition of the negative signaling pathway and so on.
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