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Jatrorrhizine can improve nerve cell injury induced by Aβ 25-35, acting through miR-223-3p/HDAC4 axis
1Zhaoqing Medical College Zhaoqing, Guangdong Province, China.
Objective:
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.
Methods:
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.
Results:
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).
Conclusion:
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.
