Emodin attenuates TNF-α-induced apoptosis and autophagy in mouse C2C12 myoblasts though the phosphorylation of Akt

Chen, Dexiu; Liu, Junshan; Lu, Lu; Huang, Yanfeng; Wang, Yanjing; Wang, Mingqing; Liu, Yangyang; Xie, Dandan; Chen, Jiebing; Diao, Jiang; Wei, Lianbo; Wang, Ming

doi:10.1016/j.intimp.2016.02.023

Cited by 41 publications

(12 citation statements)

References 62 publications

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“…But, the phenomenon was evidently abated by EMO disposition. The results were partly similar to Chen et al uncovered that EMO lightened TNF-a-induced apoptosis and autophagy in mouse C2C12 myoblasts [28]. These observations indicated that EMO weakened hypoxia-triggered PC-12 cell injury.…”

Section: Discussionsupporting

confidence: 88%

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

Cao¹,

Fang

Jia

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Emodin (EMO) possesses extensive pharmacological activities, which has been proven to exert the protective impact in diverse nervous system diseases. Nonetheless, whether EMO emerges a neuro-protective activity in hypoxic-evoked ischemic brain injury is still further probed. The intention of the research is to disclose whether EMO emerges neuro-protective activity in hypoxic-evoked ischemic brain injury. PC-12 received hypoxia administration, and then cell viability, apoptosis and autophagy were estimated. After EMO disposition, the above-involved cellular processes were evaluated again. MiR-25 functions in EMO-affected cells were also estimated. The interrelation between miR-25 and neurofilament light-chain polypeptide gene (NEFL) and the conceivable roles of NEFL in hypoxia-disposed cells were investigated. The latent mechanism was uncovered by mTOR and Notch pathways determination. Hypoxia triumphantly triggered apoptosis and autophagy, but EMO repressed these functions in PC-12 cells. Increased miR-25 was induced by EMO, and inhibited miR-25 abated the impacts of EMO on hypoxia-disposed PC-12 cells. NEFL as a neoteric target gene of miR-25 was predicated, and overexpressed NEFL annulled the functions of EMO in hypoxia-injured cells. EMO activated mTOR and Notch pathways through repressing NEFL. The investigations corroborated that EMO weakened hypoxia-triggered injury via elevating miR-25 by targeting NEFL in PC-12 cells.

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Section: Discussionsupporting

confidence: 88%

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

Cao¹,

Fang

Jia

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Thus, the protective effect of emodin against CLP-induced intestinal barrier injury can be partially explained by the increased expression of TJ proteins. In recent years, numerous scientific reports described that emodin has an anti-inflammatory effect and can reduce the expression of the inflammatory factor TNF-α (55)(56)(57). Compared with expression in the corresponding CLP group, the protein expression levels of claudin-3 in the CLP + emodin group showed a continuous and uniform distribution, with a smoother edge and an enhanced positive signal.…”

Section: Discussionmentioning

confidence: 91%

Protective effect of emodin on intestinal epithelial tight junction barrier integrity in rats with sepsis induced by cecal ligation and puncture

Guo

Zhang

et al. 2020

Exp Ther Med

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Αbstract. The present study investigated the protective effects of emodin on intestinal epithelial tight junction (TJ) barrier integrity in cecal ligation and puncture (CLP)-induced septic rats and its possible mechanisms of action. Healthy male Sprague-Dawley rats were randomly divided into three groups (n=20 per group): Sham group, CLP group and CLP + emodin group. Animals were sacrificed at 12 and 24 h after the model was established. Abdominal aortic blood and specimens of the ileum were harvested for analysis. The histopathological changes in intestinal mucosa and the ultrastructures of intestinal epithelial cells were investigated using light microscopy and transmission electron microscopy. The integrity of the intestinal barrier was assessed by examining plasma diamine oxidase (DAO) levels and the ratio of urine lactulose to mannitol (L/M). The levels of the intestinal TJ proteins claudin-3, zonula occludens (ZO)-1 and occludin were detected using immunohistochemistry, western blotting and reverse transcription-quantitative PCR. The results showed that the pathological damage to intestinal mucosa and the intestinal tissue injury score in the CLP + emodin group were significantly reduced compared to those of the CLP group, and the differences were more obvious at 24 h compared with 12 h. DAO activity and the L/M ratio in the emodin pre-treatment group decreased significantly at 24 h compared with the CLP groups. The protein and mRNA levels of the TJ proteins claudin-3, ZO-1 and occludin in the emodin pre-treatment groups at 12 and 24 h were increased, while occludin mRNA level was found to be decreased compared with the CLP groups. The present study suggested that emodin may significantly reduce the damage to the intestinal epithelial barrier in sepsis, inhibit intestinal barrier permeability and protect intestinal barrier integrity. Emodin may protect intestinal barrier integrity by elevating expression levels of the TJ proteins claudin-3, ZO-1 and occludin in CLP rats.

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“…This is based on studies where reduced autophagosome formation and maturation were observed with TNFα blockers 145,153 . It is a chain of events where TNFα-associated upregulation of autophagy (by inducing ROS production) is mediated by activating the Jun kinase pathway and inhibiting the Akt pathway 145,157 . Similarly, in vitro experiments conducted in fibrotic kidney and hepatoma cells have confirmed that another inflammatory cytokine, TGFβ, also upregulates autophagic genes such as Beclin 1, Atg5, and Atg7 145,158 .…”

Section: Association Of Autophagy and Inflammatory Phenotype In Metsmentioning

confidence: 99%

Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system

et al. 2020

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Metabolic syndrome (MetS) is a complex, emerging epidemic which disrupts the metabolic homeostasis of several organs, including liver, heart, pancreas, and adipose tissue. While studies have been conducted in these research areas, the pathogenesis and mechanisms of MetS remain debatable. Lines of evidence show that physiological systems, such as the renin-angiotensin system (RAS) and autophagy play vital regulatory roles in MetS. RAS is a pivotal system known for controlling blood pressure and fluid balance, whereas autophagy is involved in the degradation and recycling of cellular components, including proteins. Although RAS is activated in MetS, the interrelationship between RAS and autophagy varies in glucose homeostatic organs and their cross talk is poorly understood. Interestingly, autophagy is attenuated in the liver during MetS, whereas autophagic activity is induced in adipose tissue during MetS, indicating tissue-specific discordant roles. We discuss in vivo and in vitro studies conducted in metabolic tissues and dissect their tissue-specific effects. Moreover, our review will focus on the molecular mechanisms by which autophagy orchestrates MetS and the ways future treatments could target RAS in order to achieve metabolic homeostasis. Facts • The renin-angiotensin system (RAS) is a pivotal endocrine system classically known for controlling blood pressure and fluid balance.

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Emodin attenuates TNF-α-induced apoptosis and autophagy in mouse C2C12 myoblasts though the phosphorylation of Akt

Cited by 41 publications

References 62 publications

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

Protective effect of emodin on intestinal epithelial tight junction barrier integrity in rats with sepsis induced by cecal ligation and puncture

Autophagy in metabolic syndrome: breaking the wheel by targeting the renin–angiotensin system

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