Reduced lifespan of mice lacking catalase correlates with altered lipid metabolism without oxidative damage or premature aging

Pérez-Estrada, José Raúl; Hernández-García, David; Leyva-Castro, Francisco; Ramos-León, Javier; Cuevas-Benítez, Osiris; Dı́az-Muñoz, Mauricio; Castro-Obregón, Susana; Ramírez-Solís, Ramiro; García, Celina; Covarrubias, Luis

doi:10.1016/j.freeradbiomed.2019.02.016

Cited by 27 publications

(24 citation statements)

References 60 publications

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“…The harmful H 2 O 2 also can be degraded into O 2 and H 2 O by CAT and GSH-Px ( 42 ). Catalase exists in the cytoplasm and can reduce fat accumulation without oxidative damage and control the peroxisomal H 2 O 2 that degrades hepatic fatty acids, thus maintaining the optimal metabolic balance ( 43 ).…”

Section: Discussionmentioning

confidence: 99%

Hepatoprotective Effect of Lactobacillus plantarum HFY09 on Ethanol-Induced Liver Injury in Mice

et al. 2021

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Lactobacillus plantarum is a bacterial strain that is used as a probiotic with health-promoting effects. Our study investigated the hepatoprotective effect of Lactobacillus plantarum HFY09 (LP-HFY09) in mice with ethanol-induced liver injury. The protection afforded by LP-HFY09 was evaluated by observing the morphology of hepatic tissue and measuring liver lipid indexes and function indexes, levels of anti-oxidative enzymes, and anti-inebriation enzymes, as well as oxidative metabolism-related gene expression. Gavage administration of LP-HFY09 [1 × 109 CFU/kg body weight (bw)] limited the loss of bw, alcohol damage to the liver, and maintained the normal hepatic tissue morphology. Lactobacillus plantarum HFY09 intervention in ethanol-induced mice led to decreases in serum triglyceride (TG), total cholesterol (TC), aspartic transaminase, alanine transaminase, hyaluronidase (HAase), and precollagen III (PC III), and increases in liver alcohol dehydrogenase (ADH), and acetaldehyde dehydrogenase (ALDH). Lactobacillus plantarum HFY09 assisted with alleviating inflammation by elevating the level of interleukin 10 (IL-10) and decreasing the levels of pro-inflammatory factors [IL-6, IL-1β, and tumor necrosis factor-α (TNF)-α]. Lactobacillus plantarum HFY09 significantly elevated hepatic levels of superoxide dismutase (SOD) and glutathione (GSH), and decreased liver malondialdehyde (MDA) from 3.45 to 1.64 nmol/mg protein. Lactobacillus plantarum HFY09 exhibited an overall strong regulatory effect on liver protection when compared to that of commercial Lactobacillus delbrueckii subsp. bulgaricus. The hepatoprotective effect of LP-HFY09 was reflected by the upregulated expression of peroxisome proliferator activated-receptors α, SOD1, SOD2, glutathione peroxidase (GSH-Px), nicotinamide adenine dinucleotide phosphate (NADPH), and catalase (CAT), and the downregulated expression of cyclooxygenase-1 (COX1), c-Jun N-terminal kinase (JNK), and extracellular regulated protein kinases (ERK). Administration of LP-HFY09 at a concentration of 1.0 × 109 CFU/kg bw could be a potential intervention, for people who frequently consume alcohol.

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Section: Discussionmentioning

confidence: 99%

Hepatoprotective Effect of Lactobacillus plantarum HFY09 on Ethanol-Induced Liver Injury in Mice

et al. 2021

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“…GPx is a family of selenoproteins that are responsible for the conversion of H 2 O 2 and other organic peroxides, to water and oxygen [54]. CAT is a common antioxidant enzyme present abundantly in liver, lungs, and kidneys [55]. CAT plays an important role in protecting organisms against oxidative damage caused by ROS by degrading hydrogen peroxide [56].…”

Section: Discussionmentioning

confidence: 99%

CPUY192018, a potent inhibitor of the Keap1-Nrf2 protein-protein interaction, alleviates renal inflammation in mice by restricting oxidative stress and NF-κB activation

et al. 2019

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The Keap1-Nrf2-ARE pathway regulates the constitutive and inducible transcription of various genes that encode detoxification enzymes, antioxidant proteins and anti-inflammatory proteins and has pivotal roles in the defence against cellular oxidative stress. In this study, we investigated the therapeutic potential of CPUY192018 , a potent small-molecule inhibitor of the Keap1-Nrf2 protein-protein interaction (PPI), in renal inflammation. In human proximal tubular epithelial HK-2 cells, CPUY192018 treatment significantly increased Nrf2 protein level and Nrf2 nuclear translocation, which enhanced Nrf2-ARE transcription capacity and the downstream protein content in a Nrf2 dependent manner. In lipopolysaccharide (LPS)-challenged human HK-2 cells, CPUY192018 exhibited cytoprotective effects by enhancing the Nrf2-ARE regulated antioxidant system and diminished the LPS-induced inflammatory response by hindering the ROS-mediated activation of the NF-κB pathway. In the LPS-induced mouse model of chronic renal inflammation, by activating Nrf2, CPUY192018 treatment balanced renal oxidative stress and suppressed inflammatory responses. Hence, administration of CPUY192018 reduced kidney damage and ameliorated pathological alterations of the glomerulus. Taken together, our study suggested that small-molecule Keap1-Nrf2 PPI inhibitors can activate the Nrf2-based cytoprotective system and protect the kidney from inflammatory injury, raising a potential application of Keap1-Nrf2 PPI inhibitors in the treatment of inflammatory kidney disorders.

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“…CAT, in the cytoplasm, maintains optimal metabolic balance by reducing fat accumulation without oxidative damage. It also degrades fatty acids in the liver by controlling the peroxisomal H 2 O 2 (Pérez‐Estradaa et al., 2019). SOD is the first detoxification enzyme, eliminating superoxide radicals.…”

Section: Discussionmentioning

confidence: 99%

“…SOD2 eliminates superoxide radicals by catalyzing the dismutation of superoxide. The H 2 O 2 produced by SOD2 action is effectively reduced by CAT, GSH, and GSH‐PX into H 2 O (Pérez‐Estradaa et al., 2019; Vuolo et al., 2019), or converted into H 2 and O 2 by SOD1 (Cruciani‐Guglielmacci & Magnan, 2017). In our study, LP‐CQPC03 could reduce TC, TG, and LDL‐C, and increase HDL‐C in both liver and serum.…”

Section: Discussionmentioning

confidence: 99%

Regulating effect ofLactobacillus plantarumCQPC03 on lipid metabolism in high‐fat diet‐induced obesity in mice

et al. 2020

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Probiotics are regard as safety approaches for preventing and treating some chronic diseases. This study investigated the regulating effect of Lactobacillus plantarum CQPC03 (LP-CQPC03) on lipid metabolism in high-fat diet (HFD)-induced obesity in mice. The results showed that administration of LP-CQPC03 at a concentration of 1.0 × 10 9 CFU/kg body weight inhibits HFD-induced obesity and improves lipid metabolism in the liver and serum. LP-CQPC03 intervention attenuated obesityinduced hepatic tissue damage, led decreases in hepatic triglyceride (42.02 mmol/ gprot), total cholesterol (3.85 mmol/gprot), and LDL-C (1.03 mmol/gprot), and an increase in HDL-C (1.07 mmol/gprot). The same tendencies were observed in serum of HFD-fed mice. LP-CQPC03 intervention led a decrease in serum levels of aspartic transaminase, alanine transaminase, and alkaline phosphatase. LP-CQPC03 alleviated inflammation by increasing the level of interleukin (IL)-4

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Reduced lifespan of mice lacking catalase correlates with altered lipid metabolism without oxidative damage or premature aging

Cited by 27 publications

References 60 publications

Hepatoprotective Effect of Lactobacillus plantarum HFY09 on Ethanol-Induced Liver Injury in Mice

Hepatoprotective Effect of Lactobacillus plantarum HFY09 on Ethanol-Induced Liver Injury in Mice

CPUY192018, a potent inhibitor of the Keap1-Nrf2 protein-protein interaction, alleviates renal inflammation in mice by restricting oxidative stress and NF-κB activation

Regulating effect ofLactobacillus plantarumCQPC03 on lipid metabolism in high‐fat diet‐induced obesity in mice

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