Protective effects of Lactobacillus fermentum U-21 against paraquat-induced oxidative stress in Caenorhabditis elegans and mouse models

2020 ◽  
Vol 36 (7) ◽  
Author(s):  
Maria Marsova ◽  
Elena Poluektova ◽  
Maya Odorskaya ◽  
Alexander Ambaryan ◽  
Alexander Revishchin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Mouse Models ◽  
Lactobacillus Fermentum ◽  
Protective Effects

scholarly journals Lipopolysaccharide exposure induces oxidative damage in Caenorhabditis elegans: protective effects of carnosine

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Jing Ma ◽  
Xiaoyuan Xu ◽  
Ranran Wang ◽  
Haijing Yan ◽  
Huijuan Yao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
Protective Effects ◽  
Related Gene ◽  
Rt Pcr ◽  
C Elegans ◽  
Apoptosis Related Gene

Abstract Background The present study was designed to investigate the protective effects and mechanisms of carnosine on lipopolysaccharide (LPS)-induced injury in Caenorhabditis elegans. Methods C. elegans individuals were stimulated for 24 h with LPS (100 μg/mL), with or without carnosine (0.1, 1, 10 mM). The survival rates and behaviors were determined. The activities of superoxide dismutase (SOD), glutathione reductase (GR), and catalase (CAT) and levels of malondialdehyde (MDA) and glutathione (GSH) were determined using the respective kits. Reverse transcription polymerase chain reaction (RT-PCR) was performed to validate the differential expression of sod-1, sod-2, sod-3, daf-16, ced-3, ced-9, sek-1, and pmk-1. Western blotting was used to determine the levels of SEK1, p38 mitogen-activated protein kinase (MAPK), cleaved caspase3, and Bcl-2. C. elegans sek-1 (km2) mutants and pmk-1 (km25) mutants were used to elucidate the role of the p38 MAPK signaling pathway. Results Carnosine improved the survival of LPS-treated C. elegans and rescued behavioral phenotypes. It also restrained oxidative stress by decreasing MDA levels and increasing SOD, GR, CAT, and GSH levels. RT-PCR results showed that carnosine treatment of wild-type C. elegans up-regulated the mRNA expression of the antioxidant-related genes sod-1, sod-2, sod-3, and daf-16. The expression of the anti-apoptosis-related gene ced-9 and apoptosis-related gene ced-3 was reversed by carnosine. In addition, carnosine treatment significantly decreased cleaved caspase3 levels and increased Bcl-2 levels in LPS-treated C. elegans. Apoptosis in the loss-of-function strains of the p38 MAPK signaling pathway was suppressed under LPS stress; however, the apoptotic effects of LPS were blocked in the sek-1 and pmk-1 mutants. The expression levels of sek-1 and pmk-1 mRNAs were up-regulated by LPS and reversed by carnosine. Finally, the expression of p-p38MAPK and SEK1 was significantly increased by LPS, which was reversed by carnosine. Conclusion Carnosine treatment protected against LPS injury by decreasing oxidative stress and inhibiting apoptosis through the p38 MAPK pathway.

scholarly journals The Foodborne Strain Lactobacillus fermentum MBC2 Triggers pept-1-Dependent Pro-Longevity Effects in Caenorhabditis elegans

2019 ◽  
Vol 7 (2) ◽  
pp. 45 ◽  
Author(s):  
Emily Schifano ◽  
Paola Zinno ◽  
Barbara Guantario ◽  
Marianna Roselli ◽  
Sante Marcoccia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Acid Tolerance ◽  
Lactobacillus Fermentum ◽  
In Vivo Model ◽  
Aging Effects ◽  
Pumping Rate ◽  
Gut Colonization

Lactic acid bacteria (LAB) are involved in several food fermentations and many of them provide strain-specific health benefits. Herein, the probiotic potential of the foodborne strain Lactobacillus fermentum MBC2 was investigated through in vitro and in vivo approaches. Caenorhabditis elegans was used as an in vivo model to analyze pro-longevity and anti-aging effects. L. fermentum MBC2 showed a high gut colonization capability compared to E. coli OP50 (OP50) or L. rhamnosus GG (LGG). Moreover, analysis of pumping rate, lipofuscin accumulation, and body bending showed anti-aging effects in L. fermentum MBC2-fed worms. Studies on PEPT-1 mutants demonstrated that pept-1 gene was involved in the anti-aging processes mediated by this bacterial strain through DAF-16, whereas the oxidative stress protection was PEPT-1 independent. Moreover, analysis of acid tolerance, bile tolerance, and antibiotic susceptibility were evaluated. L. fermentum MBC2 exerted beneficial effects on nematode lifespan, influencing energy metabolism and oxidative stress resistance, resulted in being tolerant to acidic pH and able to adhere to Caco-2 cells. Overall, these findings provide new insight for application of this strain in the food industry as a newly isolated functional starter. Furthermore, these results will also shed light on C. elegans molecular players involved in host-microbe interactions.

scholarly journals Oxidative Stress in Caenorhabditis elegans: Protective Effects of Spartin

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0130455 ◽  
Author(s):  
Timothy Truong ◽  
Zachary A. Karlinski ◽  
Christopher O’Hara ◽  
Maleen Cabe ◽  
Hongkyun Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Protective Effects

Oxidative stress in Caenorhabditis elegans : protective effects of the Omega class glutathione transferase ( GSTO‐1 )

2007 ◽  
Vol 22 (2) ◽  
pp. 343-354 ◽  
Author(s):  
Cora Burmeister ◽  
Kai LÜersen ◽  
Alexander Heinick ◽  
Ayman Hussein ◽  
Marzena Domagalski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Glutathione Transferase ◽  
Protective Effects

scholarly journals Protective effects of novel organic selenium compounds against oxidative stress in the nematode Caenorhabditis elegans

2015 ◽  
Vol 2 ◽  
pp. 961-967 ◽  
Author(s):  
Sílvio Terra Stefanello ◽  
Priscila Gubert ◽  
Bruna Puntel ◽  
Caren Rigon Mizdal ◽  
Marli Matiko Anraku de Campos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Protective Effects ◽  
Nematode Caenorhabditis Elegans ◽  
Selenium Compounds ◽  
Organic Selenium

scholarly journals Neuroprotective Effects of Glochidion zeylanicum Leaf Extract against H2O2/Glutamate-Induced Toxicity in Cultured Neuronal Cells and Aβ-Induced Toxicity in Caenorhabditis elegans

Biology ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 800
Author(s):  
Chatrawee Duangjan ◽  
Panthakarn Rangsinth ◽  
Shaoxiong Zhang ◽  
Xiaojie Gu ◽  
Michael Wink ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Leaf Extract ◽  
Neuronal Cells ◽  
Antioxidant Properties ◽  
Ros Generation ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Antioxidant Genes ◽  
Age Related

Oxidative stress plays a crucial role in the development of age-related neurodegenerative diseases. Previously, Glochidion zeylanicum methanol (GZM) extract has been reported to have antioxidant and anti-aging properties. However, the effect of GZM on neuroprotection has not been reported yet; furthermore, the mechanism involved in its antioxidant properties remains unresolved. The study is aimed to demonstrate the neuroprotective properties of GZM extract and their underlying mechanisms in cultured neuronal (HT-22 and Neuro-2a) cells and Caenorhabditis elegans models. GZM extract exhibited protective effects against glutamate/H2O2-induced toxicity in cultured neuronal cells by suppressing the intracellular reactive oxygen species (ROS) generation and enhancing the expression of endogenous antioxidant enzymes (SODs, GPx, and GSTs). GZM extract also triggered the expression of SIRT1/Nrf2 proteins and mRNA transcription of antioxidant genes (NQO1, GCLM, and EAAT3) which are the master regulators of cellular defense against oxidative stress. Additionally, GZM extract exhibited protective effects to counteract β-amyloid (Aβ)-induced toxicity in C. elegans and promoted neuritogenesis properties in Neuro-2a cells. Our observations suggest that GZM leaf extract has interesting neuritogenesis and neuroprotective potential and can possibly act as potential contender for the treatment of oxidative stress-induced Alzheimer’s disease (AD) and related neurodegenerative conditions; however, this needs to be studied further in other in vivo systems.

scholarly journals Tanshinone IIA Protects against Acute Pancreatitis in Mice by Inhibiting Oxidative Stress via the Nrf2/ROS Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Weiwei Chen ◽  
Chenchen Yuan ◽  
Yingying Lu ◽  
Qingtian Zhu ◽  
Xiaojie Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Pancreatitis ◽  
Mouse Models ◽  
Serum Amylase ◽  
Sodium Taurocholate ◽  
Pancreatic Tissue ◽  
Tanshinone Iia ◽  
Heme Oxygenase 1 ◽  
Protective Effects ◽  
Nrf2 Knockout

Background. Danshen (Salvia miltiorrhiza Bunge) and its main active component Tanshinone IIA (TSA) are clinically used in China. However, the effects of TSA on acute pancreatitis (AP) and its potential mechanism have not been investigated. In this study, our objective was to investigate the protective effects of TSA against AP via three classic mouse models. Methods. Mouse models of AP were established by caerulein, sodium taurocholate, and L-arginine, separately. Pancreatic and pulmonary histopathological characteristics and serum amylase and lipase levels were evaluated, and changes in oxidative stress injury and the ultrastructure of acinar cells were observed. The reactive oxygen species (ROS) inhibitor N-Acetylcysteine (NAC) and nuclear factor erythroid 2-related factor 2 (Nrf2) knockout mice were applied to clarify the protective mechanism of the drug. Results. In the caerulein-induced AP model, TSA administration reduced serum amylase and lipase levels and ameliorated the histopathological manifestations of AP in pancreatic tissue. Additionally, TSA appreciably decreased ROS release, protected the structures of mitochondria and the endoplasmic reticulum, and increased the protein expression of Nrf2 and heme oxygenase 1 of pancreatic tissue. In addition, the protective effects of TSA against AP were counteracted by blocking the oxidative stress (NAC administration and Nrf2 knockout in mice). Furthermore, we found that TSA protects pancreatic tissue from damage and pancreatitis-associated lung injury in two additional mouse models induced by sodium taurocholate and by L-arginine. Conclusion. Our data confirmed the protective effects of TSA against AP in mice by inhibiting oxidative stress via the Nrf2/ROS pathway.

Protective Effects of Baicalin on Lipopolysaccharide-Induced Injury in Caenorhabditis elegans

Pharmacology ◽  
2019 ◽  
Vol 105 (1-2) ◽  
pp. 109-117 ◽  
Author(s):  
Jing Ma ◽  
Ranran Wang ◽  
Haijing Yan ◽  
Renjie Xu ◽  
Ajing Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Survival Rates ◽  
Nuclear Factor Κb ◽  
Enzyme Linked Immunosorbent Assay ◽  
Experimental Sepsis ◽  
Protective Effects ◽  
Sod Activity ◽  
C Elegans ◽  
Tnf Α

Objectives: Sepsis-induced inflammation injury and oxidative stress are well known causes of mortality. The anti-inflammatory effects of baicalin have been proposed in a mouse model of experimental sepsis. Here, we investigated its protective effects and associated mechanisms with respect to lipopolysaccharide (LPS)-induced injury in Caenorhabditis elegans. Methods: Worms were stimulated by LPS (100 μg/mL), with baicalin (1, 10, 100 μmol/L), for 24 h. Animal survival rates and behaviors (reversal and omega turn) were then determined. Further, levels of the inflammatory cytokines interleukin 6 (IL-6), IL-1, and tumor necrosis factor (TNF)-α were detected by enzyme-linked immunosorbent assay. Western blotting was also performed to determine the protein expression levels of Toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB), Bax, and Bcl-2. The activities of malondialdehyde (MDA) and superoxide dismutase (SOD) contents were determined using corresponding kits. Results: Baicalin (10, 100 μmol/L) improved LPS-stimulated C. elegans survival and rescued behavioral phenotypes. It also suppressed the oxidative stress related to LPS injury by decreasing MDA levels and increasing SOD activity. Moreover, the inflammatory response was inhibited as evidenced by decreased levels of cytokines including IL-6, IL-1, and TNF-α. In addition, baicalin treatment significantly decreased cleaved Bax levels and increased Bcl-2 expression in C. elegans treated with LPS. Simultaneously, the expression of NF-κB and TLR4 was significantly decreased. Conclusion: Baicalin treatment protects against LPS-induced injury by decreasing oxidative stress, repressing the inflammatory cascade, and inhibiting apoptosis.

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