Jatrorrhizine can improve nerve cell injury induced by Aβ 25-35, acting through miR-223-3p/HDAC4 axis

JAT can improve the nerve injury induced by Aβ 25-35 by up-regulating miR-223-3p and inhibiting the HDAC4 expression, suppress apoptosis and OS, and induce proliferation. This research further clarified the mechanism of JAT in AD.

SH-SY5Y cells were treated with Aβ 25-35 to simulate nerve injury in the pathogenesis of Alzheimer's disease (AD), and JAT-treated SH-SY5Y cells were assessed for HDAC4 and miR-223-3p. The HDAC4 and miR-223-3p levels were tested by qRT-PCR. Proliferation was determined through MTT. Apoptosis was assessed by flow cytometry, and the related indexes of oxidative stress (OS) were examined by an OS kit.

The purpose of this research is to probe the mechanism of Jatrorrhizine (JAT) improving Aβ 25-35-induced nerve cell injury through the miR-223-3p/HDAC4 axis.

Compared with AD group, OD value increased, apoptosis rate decreased, and OS was inhibited in the AD+JAT group (all P<0.05). In SH-SY5Y cells, miR-223-3p can specifically inhibit the HDAC4 expression. The miR-223-3p expression increased and HDAC4 decreased after JAT acted on SH-SY5Y cells stimulated by Aβ 25-35 (all P<0.05). The addition of over-expression HDAC4 vector or miR-223-3p inhibitor could inhibit proliferation, and promote apoptosis and OS on the basis of JAT (all P<0.05). In addition, over-expressing miR-223-3p can suppress over-expressed HDAC4's effects on proliferation, apoptosis, and OS of SH-SY5Y cells (all P<0.05).