Possible Protective Effects of high- versus low- dose of lutein in combination with irinotecan on Liver of Rats: Role of Oxidative Stress and Apoptosis

NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome-mediated pyroptosis is a crucial event in the preeclamptic pathogenesis, tightly linked with the uteroplacental TLR4/NF-κB signaling. Trophoblastic glycometabolism reprogramming has now been noticed in the preeclampsia pathogenesis, plausibly modulated by the TLR4/NF-κB signaling as well. Intriguingly, cellular pyroptosis and metabolic phenotypes may be inextricably linked and interacted. Metformin (MET), a widely accepted NF-κB signaling inhibitor, may have therapeutic potential in preeclampsia while the underlying mechanisms remain unclear. Herein, we investigated the role of MET on trophoblastic pyroptosis and its relevant metabolism reprogramming. The safety of pharmacologic MET concentration to trophoblasts was verified at first, which had no adverse effects on trophoblastic viability. Pharmacological MET concentration suppressed NLRP3 inflammasome-induced pyroptosis partly through inhibiting the TLR4/NF-κB signaling in preeclamptic trophoblast models induced via low-dose lipopolysaccharide. Besides, MET corrected the glycometabolic reprogramming and oxidative stress partly via suppressing the TLR4/NF-κB signaling and blocking transcription factor NF-κB1 binding on the promoter PFKFB3, a potent glycolytic accelerator. Furthermore, PFKFB3 can also enhance the NF-κB signaling, reduce NLRP3 ubiquitination, and aggravate pyroptosis. However, MET suppressed pyroptosis partly via inhibiting PFKFB3 as well. These results provided that the TLR4/NF-κB/PFKFB3 pathway may be a novel link between metabolism reprogramming and NLRP3 inflammasome-induced pyroptosis in trophoblasts. Further, MET alleviates the NLRP3 inflammasome-induced pyroptosis, which partly relies on the regulation of TLR4/NF-κB/PFKFB3-dependent glycometabolism reprogramming and redox disorders. Hence, our results provide novel insights into the pathogenesis of preeclampsia and propose MET as a potential therapy.

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Evaluation of renal protective effects of the green-tea (EGCG) and red grape resveratrol: role of oxidative stress and inflammatory cytokines

Natural Product Research ◽

10.1080/14786419.2010.533669 ◽

2011 ◽

Vol 25 (8) ◽

pp. 850-856 ◽

Cited By ~ 35

Author(s):

A.M. El-Mowafy ◽

H.A. Salem ◽

M.M. Al-Gayyar ◽

M.E. El-Mesery ◽

M.F. El-Azab

Keyword(s):

Oxidative Stress ◽

Green Tea ◽

Inflammatory Cytokines ◽

Protective Effects ◽

Red Grape

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Melatonin reduces oxidative damage in mouse granulosa cells via restraining JNK-dependent autophagy

Reproduction ◽

10.1530/rep-18-0002 ◽

2018 ◽

Vol 155 (3) ◽

pp. 307-319 ◽

Cited By ~ 7

Author(s):

Yan Cao ◽

Ming Shen ◽

Yi Jiang ◽

Shao-chen Sun ◽

Honglin Liu

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Mammalian Cells ◽

Therapeutic Strategies ◽

Oxygen Species ◽

Protective Effects ◽

Follicular Atresia ◽

Direct Role ◽

Jnk Pathway

Oxidative stress-induced granulosa cell (GCs) injury is believed to be a common trigger for follicular atresia. Emerging evidence indicates that excessive autophagy occurs in mammalian cells with oxidative damage. N-acetyl-5-methoxytrypamine (melatonin) has been shown to prevent GCs from oxidative injury, although the exact mechanism remains to be elucidated. Here, we first demonstrated that the suppression of autophagy through the JNK/BCL-2/BECN1 signaling is engaged in melatonin-mediated GCs protection against oxidative damage. Melatonin inhibited the loss of GCs viability, formation of GFP-MAP1LC3B puncta, accumulation of MAP1LC3B-II blots, degradation of SQSTM1 and the expression of BECN1, which was correlated with impaired activation of JNK during oxidative stress. On the other hand, blocking of autophagy and/or JNK also reduced the level of H2O2-induced GCs death, but failed to further restore GCs viability in the presence of melatonin. Particularly, the suppression of autophagy provided no additional protective effects when GCs were pretreated with JNK inhibitor and/or melatonin. Importantly, we found that the enhanced interaction between BCL-2 and BECN1 might be a responsive mechanism for autophagy suppression via the melatonin/JNK pathway. Moreover, blocking the downstream antioxidant system of melatonin using specific inhibitors further confirmed a direct role of melatonin/JNK/autophagy axis in preserving GCs survival without scavenging reactive oxygen species (ROS). Taken together, our findings uncover a novel function of melatonin in preventing GCs from oxidative damage by targeting JNK-mediated autophagy, which might contribute to develop therapeutic strategies for patients with ovulation failure-related disorders.

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Proanthocyanidins-Mediated Nrf2 Activation Ameliorates Glucocorticoid-Induced Oxidative Stress and Mitochondrial Dysfunction in Osteoblasts

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/9102012 ◽

2020 ◽

Vol 2020 ◽

pp. 1-14

Author(s):

Liang Chen ◽

Sun-Li Hu ◽

Jun Xie ◽

De-Yi Yan ◽

She-Ji Weng ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dysfunction ◽

Low Dose ◽

Distal Femur ◽

Therapeutic Potential ◽

Protective Effects ◽

Nrf2 Pathway ◽

Pathway Activation ◽

Nrf2 Activation ◽

Osteoblast Apoptosis

The widespread use of therapeutic glucocorticoids has increased the frequency of glucocorticoid-induced osteoporosis (GIOP). One of the potential pathological processes of GIOP is an increased level of oxidative stress and mitochondrial dysfunction, which eventually leads to osteoblast apoptosis. Proanthocyanidins (PAC) are plant-derived antioxidants that have therapeutic potential against GIOP. In our study, a low dose of PAC was nontoxic to healthy osteoblasts and restored osteogenic function in dexamethasone- (Dex-) treated osteoblasts by suppressing oxidative stress, mitochondrial dysfunction, and apoptosis. Mechanistically, PAC neutralized Dex-induced damage in the osteoblasts by activating the Nrf2 pathway, since silencing Nrf2 partly eliminated the protective effects of PAC. Furthermore, PAC injection restored bone mass and promoted the expression of Nrf2 in the distal femur of Dex-treated osteoporotic rats. In summary, PAC protect osteoblasts against Dex-induced oxidative stress and mitochondrial dysfunction via the Nrf2 pathway activation and may be a promising drug for treating GIOP.

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Protective Effects of Dietary Antioxidants against Vanadium-Induced Toxicity: A Review

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/1490316 ◽

2020 ◽

Vol 2020 ◽

pp. 1-14 ◽

Cited By ~ 5

Author(s):

Iwona Zwolak

Keyword(s):

Oxidative Stress ◽

Animal Studies ◽

Toxic Metal ◽

Protective Effects ◽

Dietary Antioxidants ◽

Vanadium Toxicity ◽

Preventive Effects

Vanadium (V) in its inorganic forms is a toxic metal and a potent environmental and occupational pollutant and has been reported to induce toxic effects in animals and people. In vivo and in vitro data show that high levels of reactive oxygen species are often implicated in vanadium deleterious effects. Since many dietary (exogenous) antioxidants are known to upregulate the intrinsic antioxidant system and ameliorate oxidative stress-related disorders, this review evaluates their effectiveness in the treatment of vanadium-induced toxicity. Collected data, mostly from animal studies, suggest that dietary antioxidants including ascorbic acid, vitamin E, polyphenols, phytosterols, and extracts from medicinal plants can bring a beneficial effect in vanadium toxicity. These findings show potential preventive effects of dietary antioxidants on vanadium-induced oxidative stress, DNA damage, neurotoxicity, testicular toxicity, and kidney damage. The relevant mechanistic insights of these events are discussed. In summary, the results of studies on the role of dietary antioxidants in vanadium toxicology appear encouraging enough to merit further investigations.

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Protective Effects of Decursin and Decursinol Angelate against Amyloid β-Protein-Induced Oxidative Stress in the PC12 Cell Line: The Role of Nrf2 and Antioxidant Enzymes

Bioscience Biotechnology and Biochemistry ◽

10.1271/bbb.100606 ◽

2011 ◽

Vol 75 (3) ◽

pp. 434-442 ◽

Cited By ~ 41

Author(s):

Li LI ◽

Wei LI ◽

Sang-Won JUNG ◽

Yong-Woo LEE ◽

Yong-Ho KIM

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzymes ◽

Pc12 Cell ◽

Amyloid Β ◽

Amyloid Β Protein ◽

Protective Effects ◽

Pc12 Cell Line ◽

Β Protein ◽

Decursinol Angelate

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A Review on the Effects of Melatonin on Fetal Protection during Pregnancy with Intrauterine Inflammation

JOURNAL OF THE KOREAN SOCIETY OF MATERNAL AND CHILD HEALTH ◽

10.21896/jksmch.2020.24.4.196 ◽

2020 ◽

Vol 24 (4) ◽

pp. 196-203

Author(s):

Jang Mee Kim ◽

Ji Yeon Lee

Keyword(s):

Oxidative Stress ◽

Pregnant Women ◽

Animal Studies ◽

Protective Effects ◽

Fetal Protection ◽

Inflammatory Drugs ◽

Anti Inflammatory ◽

The Brain ◽

Fetal Inflammatory Response

Intrauterine inflammation is defined as the inflammation of the chorion, amnion, and placenta. Untreated inflammation increases the risk of fetal inflammatory response syndrome, which may result in multiorgan diseases involving the brain, cardiovascular system, lung, eye, and intestine. Therefore, controlling inflammation is critical in pregnant women to reduce the risk of diseases. However, there are no safe and effective anti-inflammatory drugs for administration during pregnancy. Although the primary function of melatonin is to control circadian rhythms, it has protective effects against cellular insults occurring from hypoxia, oxidative stress, and inflammation. While animal studies support the effective and safe role of melatonin in improving pregnancy-related morbidities, it leaves plenty of opportunities for clinical studies investigating its anti-inflammatory, antioxidant, and protective effects against insults induced by intrauterine inflammation. Therefore, it will be worthwhile to investigate antenatal supplementation of melatonin in pregnant women with intrauterine inflammation to reduce the incidence of associated comorbidities.

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Low-concentration T-2 Toxin Attenuates Pseudorabies Virus Replication in Porcine Kidney 15 Cells

10.21203/rs.3.rs-792985/v1 ◽

2021 ◽

Author(s):

Kuankuan Xiong ◽

Lei Tan ◽

Siliang Yi ◽

Yingxin Wu ◽

Yi Hu ◽

...

Keyword(s):

Oxidative Stress ◽

Pseudorabies Virus ◽

Low Dose ◽

Cell Injury ◽

Interaction Mechanism ◽

Protective Effects ◽

Porcine Kidney ◽

Low Concentration ◽

New Ideas ◽

And Control

Abstract Pseudorabies, caused by pseudorabies virus (PRV), is the main highly infectious disease that severely affects the pig industry globally. T-2 toxin (T2), a significant mycotoxin, is widely spread in food and feeds and shows high toxicity to mammals. The potential mechanism of the interaction between viruses and toxins is of great research value because revealing this mechanism may provide new ideas for their joint prevention and control. In this study, we investigated the effect of T2 on PRV replication and the mechanism of action. The results showed that at a low dose (10 nM) T2 had no significant effect on porcine kidney 15 (PK15) cell viability. However, this T2 concentration alleviated PRV-induced cell injury and increased cell survival time. Additionally, the number of PK15 cells infected with PRV was significantly reduced by T2 treatment. Similarly, T2 significantly decreased the copy number of PRV. Investigation of the mechanism revealed that 10 nM T2 significantly inhibited PRV replication and led to downregulation of oxidative stress- and apoptosis-related genes. These results suggest that oxidative stress and apoptosis are involved in the inhibition of PRV replication in PK15 cells by low-concentration T2. Taken together, we demonstrated the protective effects of T2 against PRV infection. A low T2 concentration inhibited the replication of PRV in PK15 cells, and this process was accompanied by downregulation of by the oxidative stress and apoptosis signaling pathways. Our findings partly explain the interaction mechanism between T2 and PRV, relating to oxidative stress and apoptosis, though further research is required.

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