Chrysophanol Ameliorates Hemin-Induced Oxidative Stress and Endoplasmic Reticulum Stress by Regulating MicroRNA-320-5p/Wnt3a Pathway in HT22 Cells

Abstract

Oxidative stress, endoplasmic reticulum (ER) stress, and neuronal cell apoptosis have been considered as the main pathogenesis factors of brain injury after intracerebral hemorrhage (ICH). Chrysophanol (CHR) has been proved to have neuroprotective effects, but the role and underlying mechanisms of CHR in ICH remain unclear. HT22 cells were dealt with hemin to mimic an in vitro ICH model and then subjected to treatment with or without CHR. The cell viability, apoptosis, ER stress, and oxidative stress were evaluated by conducting the cell counting kit-8 (CCK-8), TdT-mediated dUTP nick end labeling (TUNEL) staining assays, western blot, and corresponding kit, respectively. Further, microRNA-sequencing, bioinformatic analysis, dual-luciferase reporter method, and rescue experiments were conducted to explore the molecular mechanisms of CHR alleviating hemin-induced ER in HT22 cell. Our data revealed that CHR increased cells viability, antiapoptosis, anti-ER stress, and antioxidative stress under conditions of hemin-induced HT22 cell injury. Mechanically, it was observed that Wnt3a was competitively sponged by miR-320-5p, and CHR activated β-catenin pathway by regulating miR-320-5p/Wnt3a molecular axis. Finally, results from the rescue experiment suggested that CHR inhibited hemin-induced cells apoptosis, ER stress, and oxidative stress through regulating the miR-320-5p/Wnt3a axis in HT22 cells. In conclusion, CHR prevented hemin-induced apoptosis, ER stress, and oxidative stress via inhibiting the miR-320-5p/Wnt3a/β-catenin pathway in HT22 cells. Our results certified that CHR could be served as a promising treatment for brain damage following ICH.

Egr1 promotes Nlrc4-dependent neuronal pyroptosis through phlda1 in an in-vitro model of intracerebral hemorrhage

“…In order to unravel the internal mechanism of Egr1 and Phlda1 in ICH, we first built an ICH cell model and preliminarily investigated the expression status of Egr1 and Phlda1 within ICH. We exposed HT22 cells to hemin to establish an ICH cell model, based on previous studies [20][21][22]. It was found that both the mRNA and protein levels of Egr1 and Phlda1 were upregulated in hemin-treated HT22 cells (Fig.…”

“…The cells were grown in DMEM/ F12 medium (CORNING, with 10% FBS and 1% penicillin/streptomycin) and maintained in a 5% CO 2 environment at 37 °C. To simulate ICH in vitro, cells were treated with 20 μM hemin (Sigma, California, USA) for 6 h, as previously described [20].…”

The Role of LincRNA-EPS/Sirt1/Autophagy Pathway in the Neuroprotection Process by Hydrogen against OGD/R-Induced Hippocampal HT22 Cells Injury

“…Firstly, it is notable that in vivo tests were not performed. Interestingly, many previous studies have also used cell experiments alone to investigate brain injury [33,43,55]. Therefore, the experiments in vitro can reveal the related mechanism of the neuroprotection of hydrogen at a certain level.…”

“…HT22 cell, an immortalized mouse hippocampal neuronal cell line, was subcloned from parent HT4 cells originally immortalized from cultures of primary mouse hippocampal neurons [33]. HT22 cell was obtained from the Laboratory of Anesthesiology, Southwest Medical University (Luzhou, China).…”

Retracted: Chrysophanol Ameliorates Hemin-Induced Oxidative Stress and Endoplasmic Reticulum Stress by Regulating MicroRNA-320-5p/Wnt3a Pathway in HT22 Cells

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”