ROS-Induced Hepatotoxicity under Cypermethrin: Involvement of the Crosstalk between Nrf2/Keap1 and NF-κB/iκB-α Pathways Regulated by Proteasome

Zhao, Hongjing; Wang, Yu; Liu, Yachen; Yin, Kai; Wang, Dongxu; Li, Baoying; Hou, Yu; Xing, Mingwei

doi:10.1021/acs.est.1c00515

Cited by 121 publications

(34 citation statements)

References 68 publications

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“… 25 In addition, studies have shown that Nrf2 is decoupled from Keap1 when the body is affected by ROS, interacts with antioxidant response element (ARE), regulates the activity of ARE-dependent antioxidant genes (such as SOD and GSH-Px), and maintains the homeostasis of redox. 26 Our experimental results clearly confirmed that CD could reduce the level of oxidative stress in mice with LPS-induced ALI. Furthermore, LPS-induced inflammation is regulated by a variety of immune cells.…”

Section: Discussionsupporting

confidence: 78%

Chrysosplenol D protects mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via TLR4-MAPKs/NF-κB signaling pathways

et al. 2021

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This study investigated the effect and mechanism of chrysosplenol D (CD) on LPS-induced acute lung injury in mice. Histological changes in the lungs were measured by hematoxylin-eosin staining. The levels of IL-6, IL-1β, and TNF-α in the bronchoalveolar lavage fluid were detected by ELISA. The levels of oxidative stress were detected by the cuvette assay. Immune cells in peripheral blood, the levels of reactive oxygen species, and apoptosis of primary lung cells were detected by flow cytometry. The mRNA levels of TLR4, MyD88, IL-1β, and NLRP3 were measured by quantitative real-time polymerase chain reaction. The levels of proteins in apoptosis and the TLR4-MAPKs/NF-κB signaling pathways were detected by Western blot. Hematoxylin-eosin staining showed that CD could improve lung injury; decrease the levels of inflammatory factors, oxidative stress, reactive oxygen species, and cell apoptosis; and regulate the immune system. Moreover, CD could down-regulate the mRNA levels of TLR4, MyD88, NLRP3, and IL-1β in lung, and the protein levels of Keap-1, Cleaved-Caspase-3/Caspase-3, Cleaved-Caspase-9/Caspase-9, TLR4, MyD88, p-ERK/ERK, p-JNK/JNK, p-p38/p38, p-p65/p65, NLRP3, and IL-1β, and up-regulated the levels of Bcl-2/Bax, p-Nrf2/Nrf2, and HO-1. The results suggested that CD could protect mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via the TLR4-MAPKs/NF-κB signaling pathways.

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Section: Discussionsupporting

confidence: 78%

Chrysosplenol D protects mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via TLR4-MAPKs/NF-κB signaling pathways

et al. 2021

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“…40 Our study also found that HgCl 2 inhibited TH1 cytokines and induced TH2 cytokines in the thymus and BF. Oxidative stress is always accompanied by environmental toxins, [41][42][43] especially heavy metal exposure, [44][45][46] and is an important inducer of the release of pro-inflammatory cytokines. 36 The pro-oxidative stress of Hg has been well documented by mechanisms involving attack on mitochondria, 47 binding of sulfhydryl groups, 48 promotion of ROS production, 6 and weakening of anti-oxidation capacity.…”

Section: Discussionmentioning

confidence: 99%

Antagonistic effect of selenium on mercuric chloride in the central immune organs of chickens: The role of microRNA‐183/135b‐FOXO1/TXNIP/NLRP3 inflammasome axis

Gao

Chen

Chu

et al. 2022

Environmental Toxicology

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Mercury (Hg) is a persistent environmental and industrial pollutant that accumulated in the body and induces oxidative stress and inflammation damage. Selenium (Se) has been reported to antagonize immune organs damage caused by heavy metals. Here, we aimed to investigate the prevent effect of Se on mercuric chloride (HgCl 2 )-induced thymus and bursa of Fabricius (BF) damage in chickens. The results showed that HgCl 2 caused immunosuppression by reducing the relative weight, cortical area of the thymus and BF, and the number of peripheral blood lymphocytes. Meanwhile, HgCl 2 induced oxidative stress and imbalance in cytokines expression in the thymus and BF. Further, we found that thioredoxin-interacting protein (TXNIP) and the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome mediated HgCl 2 -induced oxidative stress and inflammation. Mechanically, the targeting and inhibitory effect of microRNA (miR)-135b/183 on forkhead box O1 (FOXO1) were an upstream event for HgCl 2 -activated TXNIP/NLRP3 inflammasome pathway. Most importantly, Se effectively attenuated the aforementioned damage in the thymus and BF caused by HgCl 2 and inhibited the TXNIP/NLRP3 inflammasome pathway by reversing the expression of FOXO1 through inhibiting miR-135b/183. In conclusion, the miR-135b/183-FOXO1/TXNIP/NLRP3 inflammasome axis might be a novel mechanism for Se to antagonize HgCl 2 -induced oxidative stress and inflammation in the central immune organs of chickens. K E Y W O R D S central immune organ, FOXO1/TXNIP/NLRP3 inflammasome, mercuric chloride, microRNA, selenium | INTRODUCTIONMercury (Hg) is a toxic heavy metal that is not essential for life but widely distributed in the environment. A series of Hg pollution accidents, such as the Minamata incident in Japan and the contaminated wheat grain incident in Iraq, prompted the signing of the Minamata Convention to limit the use and release of Hg. 1 Due to small-scale gold mining, coal burning, and irrational use of agricultural chemicals have not been eliminated, residents and animals in some countries and regions are still threatened by the high risk of Hg exposure. 2,3 Epidemiological investigations have shown that Hg exposure could induce oxidative stress, inflammation, and dysfunction in tissues 4,5 and cells. 6 The immune organs are responsible for immune cell generation, differentiation, and settlement and are essential for innate and

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“…Nrf2 is an important transcription factor regulating cellular redox homeostasis. Under physiologic conditions, Nrf2 concentration is low, whereas under oxidative stress, it is activated and translocated from the cytoplasm into the nucleus [ 22 ]; this can trigger downstream target genes responsible for detoxification and elimination of harmful substances [ 23 ]. The protein expression level of Kelch-like ECH-associated protein 1 (keap1) is a negative regulator of Nrf2 [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

Streptococcus lutetiensis Induces Autophagy via Oxidative Stress in Bovine Mammary Epithelial Cells

Chen

Yang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Streptococcus lutetiensis, an emerging pathogen causing bovine mastitis, has not been well characterized. We reported that S. lutetiensis was pathogenic both in vivo and in vitro and caused inflammatory reactions in the mammary gland. However, roles of autophagy and oxidative stress in the pathogenesis of S. lutetiensis-induced mastitis are unclear. In this study, an autophagy model of S. lutetiensis-infected bovine mammary epithelial cells (bMECs) was used to assess oxidative stress and autophagy flux. Expressions of Beclin1, light chain 3II, and Sequestosome 1/p62 were elevated in bMECs after S. lutetiensis infection. In addition, autophagosome and lysosome formation confirmed autophagy occurred. Based on LysoTracker Red and acridine orange, lysosome degradation was blocked, and lower expressions of lysosomal-associated membrane protein 2, cathepsins D, and cathepsins L confirmed lysosomal damage. Concurrently, the nuclear factor erythroid 2-related factor 2 (Nrf2), kelch-like ECH-associated protein 1 (Keap1), heme oxygenase 1 (HO1), and NAD (P)H: quinone oxidoreductase 1 (NQO1), and basilic proteins associated with the Nrf2/Keap1 signaling pathway, were detected. Decreased keap1 and increased Nrf2, HO1, NQO1, and reactive oxygen species (ROS) indicated increased oxidative stress. Treatment with N-Acetyl-L-cysteine (NAC), an ROS inhibitor, decreased both oxidative stress and autophagy. Therefore, we concluded that S. lutetiensis caused intracellular oxidative stress and autophagy in bMECs. In addition, crosstalk between autophagy and oxidative stress affected the autophagic flux and blocked downstream autophagy. The Nrf2-keap1-p62 pathway participated in this process, with ROS acting upstream of these effects, interfering with normal cell functions.

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ROS-Induced Hepatotoxicity under Cypermethrin: Involvement of the Crosstalk between Nrf2/Keap1 and NF-κB/iκB-α Pathways Regulated by Proteasome

Cited by 121 publications

References 68 publications

Chrysosplenol D protects mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via TLR4-MAPKs/NF-κB signaling pathways

Chrysosplenol D protects mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via TLR4-MAPKs/NF-κB signaling pathways

Antagonistic effect of selenium on mercuric chloride in the central immune organs of chickens: The role of microRNA‐183/135b‐FOXO1/TXNIP/NLRP3 inflammasome axis

Streptococcus lutetiensis Induces Autophagy via Oxidative Stress in Bovine Mammary Epithelial Cells

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