التفاصيل البيبلوغرافية
| العنوان: |
SMND-309 promotes neuron survival through the activation of the PI3K/Akt/CREB-signalling pathway. |
| المؤلفون: |
Wang, Youlei, Zhang, Jinjin, Han, Meng, Liu, Bo, Gao, Yulin, Ma, Peng, Zhang, Songzi, Zheng, Qingyin, Song, Xiaodong |
| المصدر: |
Pharmaceutical Biology; Oct2016, Vol. 54 Issue 10, p1982-1990, 9p |
| مصطلحات موضوعية: |
CELLULAR signal transduction, PHOSPHATIDYLINOSITOL 3-kinases, NEUROPROTECTIVE agents, BRAIN-derived neurotrophic factor, FLOW cytometry, LACTATE dehydrogenase, THERAPEUTICS |
| مستخلص: |
ContextIn clinical practice, the promotion of neuron survival is necessary to recover neurological functions after the onset of stroke. ObjectiveThis study aimed to investigate the post-ischaemic neuroprotective effect of SMND-309, a novel metabolite of salvianolic acid, on differentiated SH-SY5Y cells. Materials and methodsSH-SY5Y cells were differentiated by pre-treating with 5 μM all-trans-retinoic acid for 6 d. The differentiated SH-SY5Y cells were exposed to oxygen–glucose deprivation (OGD) for 2 h and reperfusion (R) for 24 h to induce OGD/R injury. After OGD injury, differentiated SH-SY5Y cells were treated with or without SMND-309 (5, 10, 20 μM) for another 24 h. Cell viability was detected through Cell counting kit-8 assay and lactate dehydrogenase leakage assay. Apoptosis was evaluated through flow cytometry, caspase-3 activity assay. Changes in protein levels were assessed through Western blot. ResultsSMND-309 ameliorated the degree of injury in the differentiated SH-SY5Y cells by increasing cell viabilities (5 μM, 65.4% ± 4.1%; 10 μM, 69.8% ± 3.7%; 20 μM, 75.3% ± 5.1%) and by reducing LDH activity (20 μM, 2.5 fold) upon OGD/R stimulation. Annexin V-fluorescein isothiocyanate/propidium iodide staining results suggested that apoptotic rate of differentiated SH-SY5Y cells decreased from 43.8% induced by OGD/R injury to 19.2% when the cells were treated with 20 μM SMND-309. SMND-309 significantly increased the Bcl-2 level of the injured differentiated SH-SY5Y cells but decreased the caspase-3 activity of these cells by 1.6-fold. In contrast, SMND-309 did not affect the Bax level of these cells. SMND-309 evidently increased the protein expression of BDNF when Akt and CREB were activated. This function was antagonized by the addition of LY294002. ConclusionSMND-309 can prevent neuronal cell deathin vitro. This process may be related to the activation of the PI3K/Akt/CREB-signalling pathway. [ABSTRACT FROM PUBLISHER] |
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| قاعدة البيانات: |
Complementary Index |
