Selenium alleviates mercury chloride-induced liver injury by regulating mitochondrial dynamics to inhibit the crosstalk between energy metabolism disorder and NF-κB/NLRP3 inflammasome-mediated inflammation

Amelioration of mercuric chloride-induced physiologic and histopathologic alterations in rats using vitamin E and zinc chloride supplement

“…Also, selenium antagonizes mercury toxicity in the brain of chickens by promoting the signaling pathways BDNF/TrKB/PI3K/AKT and suppressing NF-kappaB ( Li et al., 2022 ). It reduces the liver damage caused by mercuric chloride by controlling mitochondrial dynamics to prevent the interaction between energy metabolism dysfunction and NF–B/NLRP3 inflammasome-mediated inflammation ( Gao et al., 2021 ). Selenium can counteract mercuric chloride-induced oxidative stress and inflammation in the central immunological organs of chickens through a new mechanism involving the miR-135b/183-FOXO1/TXNIP/NLRP3 inflammasome axis ( Gao et al., 2022 ) Muthu and Krishnamoorthy (2012) showed that vitamin E could reduce testicular injury by normalizing the antioxidant activity in the testis and declining malondialdehyde and inflammatory cytokines ( Fadda et al., 2020 ).…”

Curcumin: a potential exogenous additive for the prevention of LPS‐induced duck ileitis by the alleviation of inflammation and oxidative stress

“…40 Reportedly, the NLRP3 inflammasome is involved in the NF-κB-mediated inflammatory response in chickens. 41 Accumulating evidence indicates that Nrf2 regulates the mRNA level of TXNIP, acts as an inhibitor of TXNIP activation, and maintains a low level of TXNIP expression. 42 TXNIP can bind to NLRP3, thereby activating the NLRP3 inflammasome and inducing the activation of caspase-1 and secretion of various downstream inflammatory cytokines.…”

“…CUR is regarded as an activator of Nrf2, which plays an important role in inhibiting LPS‐induced NF‐κB activation and microglial activation caused by LPS 40 . Reportedly, the NLRP3 inflammasome is involved in the NF‐κB‐mediated inflammatory response in chickens 41 . Accumulating evidence indicates that Nrf2 regulates the mRNA level of TXNIP, acts as an inhibitor of TXNIP activation, and maintains a low level of TXNIP expression 42 .…”

Bisphenol A aggravates renal apoptosis and necroptosis in selenium‐deficient chickens via oxidative stress and PI3K/AKT pathway

“…Oxidative stress is initially produced by accumulation of reactive oxygen species (ROS) and the imbalance of the antioxidant capacity in organisms. Toxic exposure can induce oxidative stress (Miao et al, 2022; Y. Wang, Zhao et al, 2021), and further oxidative stress triggers various signaling pathways, resulting in disturbed cellular ion homeostasis, inflammatory responses, apoptosis, and necroptosis (Gao et al, 2021; Samimi et al, 2019; H. Zhao et al, 2021), of which, it is worth noting that phosphatidylinositol 3‐kinase/threonine kinase (PI3K/AKT) signaling pathway, toxic exposure‐caused oxidative stress could downregulate PI3K/AKT signaling pathway (L. X. Li et al, 2022), leading to apoptosis through B‐cell lymphoma‐2 (Bcl‐2) signaling pathway, as well as programmed necroptosis via receptor‐interacting protein kinase 1 (RIP1)/RIP3/mixed lineage kinase domain‐like protein (MLKL) signaling pathway (L. Liu et al, 2021; L. Wang et al, 2020b). K. Li et al (2020) exposed chicken to ochratoxin A, finding that ochratoxin A induced renal apoptosis via modulation of oxidative stress and PI3K/AKT signaling pathway, and J. Zhang et al (2020) found that cadmium‐induced oxidative stress in common carp lymphocytes and promoted apoptosis and necrosis through the regulation of the miR‐216a‐PI3K/AKT axis, and pesticides chlorpyrifos induced the apoptosis and necroptosis in L8824 cells through the ROS/PTEN/PI3K/AKT axis (L. Wang et al, 2020b).…”

“…Oxidative stress is initially produced by accumulation of reactive oxygen species (ROS) and the imbalance of the antioxidant capacity in organisms. Toxic exposure can induce oxidative stress (Miao et al, 2022;, and further oxidative stress triggers various signaling pathways, resulting in disturbed cellular ion homeostasis, inflammatory responses, apoptosis, and necroptosis (Gao et al, 2021;Samimi et al, 2019;, of which, it is worth noting that phosphatidylinositol 3-kinase/threonine kinase (PI3K/AKT) signaling pathway, toxic exposure-caused oxidative stress could downregulate PI3K/AKT signaling pathway (L. X. Li et al, 2022), leading to apoptosis through B-cell lymphoma-2 (Bcl-2) signaling pathway, as well as programmed necroptosis via receptorinteracting protein kinase 1 (RIP1)/RIP3/mixed lineage kinase domain-like protein (MLKL) signaling pathway (L. Liu et al, 2021;L.…”