ArticleAmerican journal of translational research2021
Jatrorrhizine can improve nerve cell injury induced by Aβ 25-35, acting through miR-223-3p/HDAC4 axis.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Review
- Effects of Jatrorrhizine on inflammatory response induced by HMolecular neurobiology · 2023Article
- Research Progress on Neuroprotective Effects of Isoquinoline Alkaloids.Molecules (Basel, Switzerland) · 2023Review
- Article
- Jatrorrhizine alleviates ulcerative colitis via regulating gut microbiota and NOS2 expression.Gut pathogens · 2022Article
- Jatrorrhizine: A Review of Sources, Pharmacology, Pharmacokinetics and Toxicity.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe 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.
methodsSH-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.
resultsCompared 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).
conclusionJAT 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.
Indexed as
Identifiers
34150044PMC8205821W3174003332What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.