Protective effects of melatonin on deoxynivalenol-induced oxidative stress and autophagy in IPEC-J2 cells

Xu, Yafei; Xie, Yunxiao; Wu, Zhengchang; Wang, Haifei; Chen, Zhenhai; Wang, Jingneng; Bao, Wenbin

doi:10.1016/j.fct.2023.113803

Cited by 8 publications

(5 citation statements)

References 42 publications

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“…20,21 Xu et al demonstrated that defects in the antioxidant system of porcine jejunal epithelial cells can induce cellular damage and inflammatory responses. 22 Disruption of autophagic flow can activate the ROS pathway, leading to apoptosis in porcine epithelial cells. 23 These findings indicate that β-CG induces intestinal damage and inflammatory responses in piglets by modulating oxidative stress-related processes.…”

Section: ■ Resultsmentioning

confidence: 99%

“…Similarly, DEPs were enriched in oxidation-associated GO terms, including oxygen carrier activity, oxygen binding, and reactive oxygen species metabolic processes. Oxidative stress refers to an imbalance between oxidation and antioxidation in the body and is frequently associated with intestinal dysfunction and damage in piglets. , Xu et al demonstrated that defects in the antioxidant system of porcine jejunal epithelial cells can induce cellular damage and inflammatory responses . Disruption of autophagic flow can activate the ROS pathway, leading to apoptosis in porcine epithelial cells .…”

Section: Discussionmentioning

confidence: 99%

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Integrated Transcriptome and Proteome Analyses of β-Conglycinin-Induced Intestinal Damage in Piglets

Li,

Zheng,

Yin

et al. 2024

J. Agric. Food Chem.

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β-conglycinin (β-CG) induces intestinal damage in piglets; however, its regulatory mechanisms are not fully understood. This study aimed to investigate the molecular mechanisms by which β-CG regulates intestinal injury in piglets through downstream genes and proteins. Our findings revealed that β-CG significantly reduced villus height while increasing the crypt depth. In addition, we analyzed the transcriptome and proteome of jejunum tissues after the β-CG treatment. In total, 382 differentially expressed genes (DEGs) and 292 differentially expressed proteins (DEPs) were identified between the treatment and the control groups. The expression levels of DEGs and DEPs were validated by using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting, respectively. The findings revealed a consistent correlation between their expression levels and transcriptomic and proteomic data. In addition, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of DEGs and DEPs revealed their enrichment in oxidation-related GOs, as well as in lysosome-related pathways. A protein−protein interaction (PPI) regulatory network was constructed based on the DEPs. The integration of transcriptomic and proteomic analyses identified six genes that were significantly different at both the transcript and the protein levels. This study provides valuable insights into the molecular mechanisms underlying β-CG-induced intestinal injury in piglets.

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Section: ■ Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Integrated Transcriptome and Proteome Analyses of β-Conglycinin-Induced Intestinal Damage in Piglets

Li,

Zheng,

Yin

et al. 2024

J. Agric. Food Chem.

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“…MLT (N-acetyl-5-methoxytryptamine) is an indoleamine hormone mainly produced and secreted by the pineal gland and is widely known as a regulator of circadian rhythms [ 32 ]. Recently, increasing evidence has shown that MLT has diverse biological functions, including antioxidant [ 33 , 34 , 35 , 36 ], anti-inflammatory [ 37 , 38 , 39 ], anti-apoptosis [ 40 , 41 ] and immunomodulation [ 42 , 43 , 44 ]. Our previous study has discovered that MLT could promote proliferation, induce autophagy, and suppress apoptosis on annulus fibrosus cells, implying a role of melatonin in alleviating IDD.…”

Section: Discussionmentioning

confidence: 99%

Medical Prospect of Melatonin in the Intervertebral Disc Degeneration through Inhibiting M1-Type Macrophage Polarization via SIRT1/Notch Signaling Pathway

et al. 2023

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The study aims to explore the medical prospect of melatonin (MLT) and the underlying therapeutic mechanism of MLT-mediated macrophage (Mφ) polarization on the function of nucleus pulposus (NP) in intervertebral disc degeneration (IDD). RAW 264.7 Mφs were induced by lipopolysaccharide (LPS) to simulate Mφ polarization and the inflammatory reaction of Mφs with or without MLT were detected. Conditioned medium (CM) collected from these activated Mφs with or without MLT treatment were further used to incubate NP cells. The oxidative stress, inflammation and extracellular matrix (ECM) metabolism in NP cells were determined. Then, the changes in SIRT1/Notch signaling were detected. The agonist (SRT1720) and inhibitor (EX527) of SIRT1 were used to further explore the association among MLT. The interaction between SIRT1 and NICD was detected by immunoprecipitation (IP). Finally, puncture-induced rat IDD models were established and IDD degrees were clarified by X-ray, MRI, H&E staining and immunofluorescence (IF). The results of flow cytometry and inflammation detection indicated that LPS could induce M1-type Mφ polarization with pro-inflammatory properties. MLT significantly inhibited the aforementioned process and inhibited M1-type Mφ polarization, accompanied by the alleviation of inflammation. Compared with those without MLT, the levels of oxidative stress, pro-inflammatory cytokines and ECM catabolism in NP cells exposed to CM with MLT were markedly downregulated in a dose-dependent manner. The inhibition of SIRT1 and the enhancement of Notch were observed in activated Mφs and they can be reversed after MLT treatment. This prediction was further confirmed by using the SRT1720 and EX527 to activate or inhibit the signaling. The interaction between SIRT1 and NICD was verified by IP. In vivo study, the results of MRI, Pfirrmann grade scores and H&E staining demonstrated the degree of disc degeneration was significantly lower in the MLT-treated groups when compared with the IDD control group. The IF data showed M1-type Mφ polarization decreased after MLT treatment. MLT could inhibit M1-type Mφ polarization and ameliorate the NP cell injury caused by inflammation in vitro and vivo, which is of great significance for the remission of IDD. The SIRT1/Notch signaling pathway is a promising target for MLT to mediate Mφ polarization.

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“…In addition, MT decreased expression of LC3B and P62 protein compared with PA group, which indicated that MT actively eliminated autophagosomes and enlarged autophagy flux. Therefore, the addition of MT before PA stress may degrade more damaged mitochondria or composition though AMPK-mTOR-Beclin-1 pathway.Apart from promoting autophagy, Xu et al (2023) and Shen et al (2018) proposedthat MT would inhibit autophagy, contributing to cells survival under conditions of oxidative stress[63,64]. Thus, there is a limitation of our work include the uncertainty about MT-induced autophagy level in all stimulus because the upregulation and downregulation of autophagy by MT is defined by types and duration of stimulating drugs.…”

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confidence: 90%

Melatonin alleviates palmitic acid–induced mitochondrial dysfunction by decreasing oxidative stress and enhancing autophagy combined in bovine endometrial epithelial cells

Wang,

Zhu,

Zhao

et al. 2024

Preprint

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Background: Negative energy balance (NEB) typically occurs in dairy cows after delivery, with those in high yielding being more likely to experience significant NEB. Such metabolic imbalance could cause ketosis, which is often accompanied by a decline in reproductive performance, but the molecular mechanism has not been fully elucidated. During excessive NEB, the body fat is extensively broken down, resulting in abnormal accumulation of non-esterified fatty acids (NEFA), represented by palmitic acid (PA), within the uterus. Such an abnormal accumulation has the potential to damage bovine endometrial epithelial cells (BEECs), while the molecular mechanisms underlying its involvement in the PA-induced injury of BEECs is poorly understood. Melatonin (MT) is recognized for its regulatory role in maintaining the homeostasis of mitochondrial reactive oxygen species (mitoROS). However, less is known about whether MT could ameliorate the damage of PA on BEECs and its molecular mechanism. Results: Our results demonstrated that 0.2 mM PA stress increased the level of cellular and mitochondrial oxidative stress. Further, we observed mitochondrial dysfunction, including an abnormal incidence of mitochondrial structure and respiratory function, reduction in mitochondrial membrane potential and mitochondrial copy number, which in turn induced apoptosis. Notably, we also found an upregulation of autophagy protein (PINK, Parkin, LC3B et al), however, the P62 protein was also increased. As we expected, 100uM MT pre-treatment attenuated PA-induced mitochondrial ROS and restored mitochondrial respiratory function. Meanwhile, pre-treated MT reversed the upregulation of P62 induced by PA and activate the AMPK-mTOR-Beclin-1 pathway, contributing to increase of autophagy and decline apoptosis. Conclusions: These findings indicate that PA could induce mitochondrial dysfunction and also enhance autophagy in BEECs. In addition, MT is hypothesized to not only reduce mitochondrial oxidative stress but also facilitate the clearance of damaged mitochondria through the regulation of autophagy pathways, thereby safeguarding the mitochondrial pool and promoting cellular viability. Our study helps better understand the molecular mechanism involved in excessive NEB's impact on the fertility outcomes of high yielding dairy cows.

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Protective effects of melatonin on deoxynivalenol-induced oxidative stress and autophagy in IPEC-J2 cells

Cited by 8 publications

References 42 publications

Integrated Transcriptome and Proteome Analyses of β-Conglycinin-Induced Intestinal Damage in Piglets

Integrated Transcriptome and Proteome Analyses of β-Conglycinin-Induced Intestinal Damage in Piglets

Medical Prospect of Melatonin in the Intervertebral Disc Degeneration through Inhibiting M1-Type Macrophage Polarization via SIRT1/Notch Signaling Pathway

Melatonin alleviates palmitic acid–induced mitochondrial dysfunction by decreasing oxidative stress and enhancing autophagy combined in bovine endometrial epithelial cells

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