Research Paper Volume 13, Issue 7 pp 9542—9565

Gastrodin ameliorates learning and memory impairment in rats with vascular dementia by promoting autophagy flux via inhibition of the Ca2+/CaMKII signal pathway

GAS alleviated CoCl2-induced autophagosome accumulation in HT22 cells. (A) HT22 was incubated with different concentrations of CoCl2 for 24 h, and cell viability was detected using the MTT assay (n=6). (B) Cells were incubated with different concentrations of GAS for 1 h and then treated with CoCl2 (200 μM) for 24 h. Cell viability was assessed via the MTT assay (n=6). (C) Representative Giemsa staining of HT22 cells (magnification, 200×; n = 3) (D) Immunoblots showing levels of LC3, p62, p-p62 (Thr349)in HT22 cells treated with various concentrations of CoCl2 (0, 100, 200, 400 and 800 μM) for 24 h. β-actin was used as the loading control. (E) HT22 cells were pretreated with GAS and BAPT-AM (0.5μM) for 1 h and then exposed to CoCl2 (200μM) for 24 h. Expression of LC3, p62, and p-p62 (Thr349) was detected by immunoblotting. β-actin was used as the loading control.

Figure 3. GAS alleviated CoCl2-induced autophagosome accumulation in HT22 cells. (A) HT22 was incubated with different concentrations of CoCl2 for 24 h, and cell viability was detected using the MTT assay (n=6). (B) Cells were incubated with different concentrations of GAS for 1 h and then treated with CoCl2 (200 μM) for 24 h. Cell viability was assessed via the MTT assay (n=6). (C) Representative Giemsa staining of HT22 cells (magnification, 200×; n = 3) (D) Immunoblots showing levels of LC3, p62, p-p62 (Thr349)in HT22 cells treated with various concentrations of CoCl2 (0, 100, 200, 400 and 800 μM) for 24 h. β-actin was used as the loading control. (E) HT22 cells were pretreated with GAS and BAPT-AM (0.5μM) for 1 h and then exposed to CoCl2 (200μM) for 24 h. Expression of LC3, p62, and p-p62 (Thr349) was detected by immunoblotting. β-actin was used as the loading control.