Bacillus amyloliquefaciens SC06 Induced AKT–FOXO Signaling Pathway-Mediated Autophagy to Alleviate Oxidative Stress in IPEC-J2 Cells

Autophagy is a conserved proteolytic mechanism, which degrades and recycles damaged organs and proteins in cells to resist external stress. Probiotics could induce autophagy; however, its underlying molecular mechanisms remain elusive. Our previous study has found that BaSC06 could alleviate oxidative stress by inducing autophagy in rats. This research aimed to verify whether Bacillus amyloliquefaciens SC06 can induce autophagy to alleviate oxidative stress in IPEC-J2 cells, as well as explore its mechanisms. IPEC-J2 cells were first pretreated with 108 CFU/mL BaSC06, and then were induced to oxidative stress by the optimal dose of diquat. The results showed that BaSC06 significantly triggered autophagy, indicated by the up-regulation of LC3 and Beclin1 along with downregulation of p62 in IPEC-J2 cells. Further analysis revealed that BaSC06 inhibited the AKT–FOXO signaling pathway by inhibiting the expression of p-AKT and p-FOXO and inducing the expression of SIRT1, resulting in increasing the transcriptional activity of FOXO3 and gene expression of the ATG5–ATG12 complex to induce autophagy, which alleviated oxidative stress and apoptosis. Taken together, BaSC06 can induce AKT–FOXO-mediated autophagy to alleviate oxidative stress-induced apoptosis and cell damage, thus providing novel theoretical support for probiotics in the prevention and treatment of oxidative damage.

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Emodin Alleviates Hydrogen Peroxide-Induced Inflammation and Oxidative Stress via Mitochondrial Dysfunction by Inhibiting the PI3K/mTOR/GSK3β Pathway in Neuroblastoma SH-SY5Y Cells

BioMed Research International ◽

10.1155/2020/1562915 ◽

2020 ◽

Vol 2020 ◽

pp. 1-12

Author(s):

Rui Li ◽

Wenzhou Liu ◽

Li Ou ◽

Feng Gao ◽

Min Li ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dysfunction ◽

Signaling Pathway ◽

Molecular Mechanisms ◽

Cell Damage ◽

Neuroblastoma Cells ◽

Inflammatory Factors ◽

Protective Mechanism ◽

Human Neuroblastoma ◽

Induced Apoptosis

Emodin is an active monomer extracted from rhubarb root, which has many biological functions, including anti-inflammation, antioxidation, anticancer, and neuroprotection. However, the protective effect of emodin on nerve injury needs to be further elucidated. The purpose of this study is to investigate the effect of emodin on the neuroprotection and the special molecular mechanism. Here, the protective activity of emodin inhibiting H2O2-induced apoptosis and neuroinflammation as well as its molecular mechanisms was examined using human neuroblastoma cells (SH-SY5Y cells). The results showed that emodin significantly enhanced cell viability, reduced cell apoptosis and LDH release. Simultaneously, emodin downregulated H2O2-induced inflammatory factors, including IL-6, NO, and TNF-α, and alleviated H2O2-induced oxidative stress and mitochondrial dysfunction in SH-SY5Y cells. In addition, emodin inhibited the activation of the PI3K/mTOR/GSK3β signaling pathway. What is more, the PI3K/mTOR/GSK3β pathway participated in the protective mechanism of emodin on H2O2-induced cell damage. Collectively, it suggests that emodin alleviates H2O2-induced apoptosis and neuroinflammation potentially by regulating the PI3K/mTOR/GSK3β signaling pathway.

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Dietary polyphenol canolol from rapeseed oil attenuates oxidative stress-induced cell damage through the modulation of the p38 signaling pathway

RSC Advances ◽

10.1039/c8ra04130j ◽

2018 ◽

Vol 8 (43) ◽

pp. 24338-24345 ◽

Cited By ~ 7

Author(s):

Xiaoyang Xia ◽

Xia Xiang ◽

Fenghong Huang ◽

Mingming Zheng ◽

Renhuai Cong ◽

...

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Rapeseed Oil ◽

Cell Damage ◽

Redox Status ◽

Cellular Redox ◽

Induced Apoptosis

Canolol extracted from rapeseed oil attenuated oxidative stress-induced apoptosis and cellular redox status imbalance by inhibition of p38 phosphorylation.

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PI3K/Akt Signaling Pathway Ameliorates Oxidative Stress-Induced Apoptosis upon Manganese Exposure in PC12 Cells

Biological Trace Element Research ◽

10.1007/s12011-021-02687-1 ◽

2021 ◽

Author(s):

Yanli Tan ◽

Hong Cheng ◽

Cheng Su ◽

Pan Chen ◽

Xiaobo Yang

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Pc12 Cells ◽

Akt Signaling ◽

Akt Signaling Pathway ◽

Manganese Exposure ◽

Induced Apoptosis

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Isorhynchophylline Protects PC12 Cells Against Beta-Amyloid-Induced Apoptosis via PI3K/Akt Signaling Pathway

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/163057 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 19

Author(s):

Yan-Fang Xian ◽

Zhi-Xiu Lin ◽

Qing-Qiu Mao ◽

Jian-Nan Chen ◽

Zi-Ren Su ◽

...

Keyword(s):

Signaling Pathway ◽

Pc12 Cells ◽

Molecular Mechanisms ◽

Glycogen Synthase ◽

Neuroprotective Effect ◽

Protective Action ◽

Protective Effects ◽

Phosphorylated Akt ◽

Induced Apoptosis

The neurotoxicity of amyloid-β(Aβ) has been implicated as a critical cause of Alzheimer’s disease. Isorhynchophylline (IRN), an oxindole alkaloid isolated fromUncaria rhynchophylla,exerts neuroprotective effect againstAβ25–35-induced neurotoxicityin vitro. However, the exact mechanism for its neuroprotective effect is not well understood. The present study aimed to investigate the molecular mechanisms underlying the protective action of IRN againstAβ25–35-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Pretreatment with IRN significantly increased the cell viability, inhibited the release of lactate dehydrogenase and the extent of DNA fragmentation inAβ25–35-treated cells. IRN treatment was able to enhance the protein levels of phosphorylated Akt (p-Akt) and glycogen synthase kinase-3β(p-GSK-3β). Lithium chloride blockedAβ25–35-induced cellular apoptosis in a similar manner as IRN, suggesting that GSK-3βinhibition was involved in neuroprotective action of IRN. Pretreatment with LY294002 completely abolished the protective effects of IRN. Furthermore, IRN reversedAβ25–35-induced attenuation in the level of phosphorylated cyclic AMP response element binding protein (p-CREB) and the effect of IRN could be blocked by the PI3K inhibitor. These experimental findings unambiguously suggested that the protective effect of IRN againstAβ25–35-induced apoptosis in PC12 cells was associated with the enhancement of p-CREB expression via PI3K/Akt/GSK-3βsignaling pathway.

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Protective Effect of Ginsenoside Rd on Military Aviation Noise-Induced Cochlear Hair Cell Damage

10.21203/rs.3.rs-673642/v1 ◽

2021 ◽

Author(s):

Xuemin Chen ◽

Yu-hui LIU ◽

Shuai-fei JI ◽

Xin-miao XUE ◽

Peng LIU ◽

...

Keyword(s):

Oxidative Stress ◽

Hair Cell ◽

Signaling Pathway ◽

Cell Damage ◽

Outer Hair Cells ◽

Ginsenoside Rd ◽

Cochlear Hair Cell ◽

Aviation Noise ◽

Military Aviation ◽

Hair Cell Damage

Abstract Background Soldiers are often exposed to high-intensity noise produced by military weapons and equipment during activities, and the incidence of noise-induced hearing loss (NIHL) in many arms is high. Oxidative stress has a significant role in the pathogenesis of NIHL, and research has confirmed that ginsenoside Rd (GSRd) suppresses oxidative stress. Therefore, we hypothesized that GSRd may attenuate NIHL and cochlear hair cell loss, induced by military aviation noise stimulation, through the Sirtuin1/proliferator-activated receptor-gamma coactivator 1α (SIRT1/PGC-1α) signaling pathway.Methods Forty-eight male guinea pigs were randomly divided into four groups: control, noise stimulation, GSRd, and glycerol. The experimental groups received military helicopter noise stimulation at 115 dB (A) for 4 h daily for five consecutive days. Hair cell damage was evaluated by using inner ear basilar membrane preparation and scanning electron microscopy. Terminal dUTP nick end labeling and immunofluorescence staining were conducted. Changes in the SIRT1/PGC-1α signaling pathway and other apoptosis-related markers in the cochleae, as well as oxidative stress parameters were used as readouts.Results Loss of outer hair cells, more disordered cilia, prominent apoptosis, and elevated free radical levels were observed in the experimental groups. GSRd treatment markedly improved morphological changes and apoptosis through decreasing Bcl-2 associated X protein (Bax) expression and increasing Bcl-2 expression. In addition, GSRd upregulated superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels, decreased malondialdehyde (MDA) levels, and enhanced the activity of SIRT1 and PGC-1α messenger ribonucleic acid and protein expression.Conclusion GSRd can improve structural and functional damage to the cochleae caused by noise. The underlying mechanisms may be associated with the SIRT1/PGC-1α signaling pathway.

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Simvastatin ameliorates cognitive impairments via inhibition of oxidative stress‑induced apoptosis of hippocampal cells through the ERK/AKT signaling pathway in a rat model of senile dementia

Molecular Medicine Reports ◽

10.3892/mmr.2017.8098 ◽

2017 ◽

Cited By ~ 1

Author(s):

Wenting Liu ◽

Yan Zhao ◽

Xinyu Zhang ◽

Jiangang Ji

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Rat Model ◽

Senile Dementia ◽

Cognitive Impairments ◽

Akt Signaling ◽

Akt Signaling Pathway ◽

Induced Apoptosis

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Mitochondrial Division Inhibitor 1 Attenuates Mitophagy in a Rat Model of Acute Lung Injury

BioMed Research International ◽

10.1155/2019/2193706 ◽

2019 ◽

Vol 2019 ◽

pp. 1-11 ◽

Cited By ~ 3

Author(s):

Xu Luo ◽

Ruimeng Liu ◽

Zhihao Zhang ◽

Zhugui Chen ◽

Jian He ◽

...

Keyword(s):

Oxidative Stress ◽

Acute Lung Injury ◽

Lung Injury ◽

Mitochondrial Dysfunction ◽

Cell Damage ◽

A549 Cells ◽

Oxygenation Index ◽

Lipid Peroxides ◽

Dry Weight ◽

Induced Apoptosis

The regulation of intracellular mitochondria degradation is mediated by mitophagy. While studies have shown that mitophagy can lead to mitochondrial dysfunction and cell damage, the role of Mdivi-1 and mitophagy remains unclear in acute lung injury (ALI) pathogenesis. In this study, we demonstrated that Mdivi-1, which is widely used as an inhibitor of mitophagy, ameliorated acute lung injury assessed by HE staining, pulmonary microvascular permeability assay, measurement of wet/dry weight (W/D) ratio, and oxygenation index (PaO2/FiO2) analysis. Then, the mitophagy related proteins were evaluated by western blot. The results indicated that LPS-induced activation of mitophagy was inhibited by Mdivi-1 treatment. In addition, we found that Mdivi-1 protected A549 cells against LPS-induced mitochondrial dysfunction. We also found that Mdivi-1 reduced pulmonary cell apoptosis in the LPS-challenged rats and protected pulmonary tissues from oxidative stress (represented by the content of superoxide dismutase, malondialdehyde and lipid peroxides in lung). Moreover, Mdivi-1 treatment ameliorated LPS-induced lung inflammatory response and cells recruitment. These findings indicate that Mdivi-1 mitigates LPS-induced apoptosis, oxidative stress, and inflammation in ALI, which may be associated with mitophagy inhibition. Thus, the inhibition of mitophagy may represent a potential therapy for treating ALI.

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