Objective: To observe the effect of catalpol on damaged mouse brain microvascular endothelial cells (bEnd.3) induced by Aβ1-42

and explore the protective mechanism. Method: The bEnd.3 cells were divided into five groups:control group

model group (Aβ1-42 20 μmol · L-1)

low

middle and high-dose catalpol groups (Aβ1-42 20 μmol · L-1+catalpol 50

200

500 μmol · L-1).Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay was used to detect the effect of catalpol on bEnd.3 cell activity induced by Aβ1-42; Hoechst33258 staining was used to evaluate the effect of catalpol on apoptosis in bEnd.3 cells induced by Aβ1-42; Western blot method was to detect relevant protein expressions of autophagy and apoptosis

Beclin-1

LC3

Bax

Bcl-2

cytochrome-C

Caspase-3

cleaved Caspase-3. Result: The result of MTT showed

catalpol had no toxic and side effect on bEnd.3 cells; MTT and Hoechst staining results showed that low

middle and high-dose catalpol groups could significantly improve the activity of bEnd.3 cells and inhibit the apoptosis induced by Aβ1-42 (P<0.05)

compared with model group; the results of Western blot showed that the ratio of Beclin-1/β-actin

LC3-Ⅱ/LC3-Ⅰ

Bax/Bcl-2

cytochrome-C/β-actin and cleaved Caspase-3/Caspase-3 obviously reduced after pretreatment with catalpol (P<0.05)

compared with model group. Conclusion: Catalpol may have the neuroprotective effect by inhibiting bEnd.3 cell apoptosis and autophagy induced by Aβ1-42.