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Treatment of SH-SY5Y cells with Barlerin (8-O-Acetyl shanzhiside methyl ester) blocks TNF-α-induced nuclear transcription factor κB (NF-κB) activation and decreases high-mobility group box-1 (HMGB-1) expression. . Treatment of H9c2 cells with Barlerin (8-O-Acetyl shanzhiside methyl ester) 9 μM blocks TNF-α-induced NF-κB phosphorylation by blocking High-mobility group box1 (HMGB1) expression.

Barlerin (8-O-Acetyl shanzhiside methyl ester) 40 mg/kg demonstrates significant neuroprotective effect even after delayed administration at 4 hr after I/R. Barlerin 40 mg/kg attenuates the histopathological damage, decreases brain swelling, inhibits NF-κB activation and reduces HMGB-1 expression in ischaemic brain tissue. Barlerin (8-O-Acetyl shanzhiside methyl ester) significantly promotes angiogenesis in the ischaemic brain and improves functional outcome after stroke. Barlerin also significantly increases vascularization compared with vehicle treatment. It increases the expression of VEGF, Ang1, phosphorylation of Tie2 and Akt VEGF. Barlerin (8-O-Acetyl shanzhiside methyl ester) significantly shortens capillary blood clotting time and reduces blood loss volume, but does not influence mice activated partial thromboplastin time, prothrombin time or thrombin time. It significantly prolongs euglobulin clot lysis time in hyperfibrinolysis mice.