China
Africa
Explore chapters and articles related to this topic
Zearalenone: Insights into New Mechanisms in Human Health
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Cornelia Braicu, Alina Andreea Zimta, Ioana Berindan-Neagoe
In ICR male mice, ZEA decreased the testosterone production in Leydig cells by disrupting the communication between estrogen receptor and nuclear receptor Nur77 [67]. In rats, Leydig cells exhibit chromatin condensation and autophagy, proven by increased levels of LC3-II and BCL-2, in an attempt to delay apoptosis; but through upregulation of BAX, caspase-3, caspase-9 and downregulation of BCL-2, ZEA induced apoptosis. Necrosis may appear, but only at high concentrations, meaning 50 g/mL [68,69]. The loss of Leydig cell viability can also be explained by the overproduction of some endoplasmic reticulum stress markers, GPR78, CHOP, and caspase-12, that resulted in misfolded proteins [69] or by reducing the quantity of glutathione (GSH), a intracellular-produced antioxidant [70]. The major effects of ZEA on the male reproductive system are summarized in Table 92.2.
Outdoor Air Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
On the other hand, ER stress and related pathways have been reported to be involved in cytotoxicity by some pesticides which can cause chemical sensitivity. Paraquat, a bipyridyl herbicide, which is suspected to increase the risk of PD following chronic exposures, has been reported to induce ER stress and trigger dopaminergic cell death by enhanced cleavage of a small ER cochaperone protein, p23, and inhibition of ERAD.177 Also, some have developed UPR as their pesticide-induced chemical sensitivity progresses. Elevated levels of ER stress biomarkers like glucose-regulated protein 78 (GPR78), ER degradation enhancing-α-mannosidase-like protein (EDEM), and C/EBP homologous protein (CHOP) has also been implicated in paraquat-induced toxicity in human neuroblastoma cells. Further, paraquat activated calpain and caspase 3 along with ER-induced cascade inositol requiring protein 1 (IRE1)/apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK).178
Flavanol-rich lychee fruit extract substantially reduces progressive cognitive and molecular deficits in a triple-transgenic animal model of Alzheimer disease
Published in Nutritional Neuroscience, 2021
Xiao Chen, Benhong Xu, Luling Nie, Kaiwu He, Li Zhou, Xinfeng Huang, Peter Spencer, Xifei Yang, Jianjun Liu
Functional proteins in the ER and proteasome of the mouse brain appear to be other targets modulated by Oligonol treatment. In this category, GRP78 binds to unfolded proteins and transfers them to proteasomes for degradation. The reported increase of GRP78 (glucose-regulated protein 78) and decrease of PSA6 in 3×Tg-AD mice implies that accumulations of unfolded proteins result from proteasomal dysfunction [43]. This observation is potentially linked with both clinical and experimental reports: (a) increased occurrence of GRP78 precedes neurofibrillary tangle formation in the hippocampus of AD patients [44]; (b) activation of the unfolded protein response (UPR) mediates tau phosphorylation [45]; (c) overexpression of APP down-regulates the proteasome α-type subunit and leads to inhibition of proteasomal degradation of RCAN1 [46], and (d) accumulation of phosphorylated tau leads to dysfunction of ubiquitin-proteasome system in synapse [47]. In contrast, Oligonol modulated the UPR by reducing GPR78 and increasing PSA6 proteins in hippocampi of 3×Tg-AD mice. Reduction of GRP78 by Oligonol is consistent with a report showing that Oligonol attenuated ER stress [11]. Additionally, Oligonol increased the heat shock proteins HSP72 and HSP74 (Table S4, p = .09 and .088, respectively). Heat shock 70 kDa forms a complex with the co-chaperone protein BAG2 and transports insoluble or phosphorylated tau to proteasomes for degradation [48]. These observations could explain the modulation of Aβ and tau pathologies (Figure 2) by Oligonol.
Rutin hydrate inhibits apoptosis in the brains of cadmium chloride-treated rats via preserving the mitochondrial integrity and inhibiting endoplasmic reticulum stress
Published in Neurological Research, 2019
Dalia G. Mostafa, Eman F. Khaleel, Rehab M. Badi, Ghada A. Abdel-Aleem, Hanaa M. Abdeen
This evidence presented in this in vivo study shows that CdCl2_induced neurotoxicity in rats is associated with sustained endoplasmic reticulum (ER) stress response as confirmed by the significant increase in mRNA and protein levels of GPR78, AFT6, Xbp_1, and CHOP, as well as, the higher protein levels of p_eIF2α and caspase_12. It also shows that the neuroprotection afforded by RH is mediated by boosting endogenous antioxidant system, preserving mitochondrial Δψm and coupling and inhibiting of CdCl2_induced ER stress. A graphical abstract to illustrate these possible mechanisms of action of the neuroprotective rule is shown in Figure 8.
Advances in research on the protective mechanisms of traditional Chinese medicine (TCM) in myocardial ischaemia-reperfusion injury
Published in Pharmaceutical Biology, 2022
Jiexin Zhang, Yonghe Hu, Han Wang, Jun Hou, Wenjing Xiao, Xudong Wen, Tingting Wang, Pan Long, Hezhong Jiang, Zhanhao Wang, Huawei Liu, Xin Chen
We found 19 species of Chinese herbs that have a regulatory effect on apoptosis (Table 4). Caspase-3, Bax, Bcl-2 and other apoptosis-related proteins can directly reflect apoptosis. Many herbs regulate these apoptosis-related proteins to inhibit apoptosis (No. 16 in Figure 1), such as Paeonia veitchii Lynch (Ranunculaceae) (Wang K and Hu 2020), Pueraria lobata (Willd.) Ohwi (Leguminosae) (Fan HX and Zhang et al. 2017), and Curcuma longa L. (Zingiberaceae) (Mohanty et al. 2006). The mitogen-activated protein kinase (MAPK) signalling pathway is an important pathway causing myocardial cell injury and apoptosis (Li et al. 2016). Two medicinal plants [Diospyros kaki Thunb. (Ebenaceae) (Meng et al. 2019), Gastrodia elata Bl. (Orchidaceae) (Zhang et al. 2019)] can reduce the rate of myocardial apoptosis and the size of MI by regulating the MAPK/ERK1/2 signalling pathway (No. 6 in Figure 1). Furthermore, ERS is a relatively newly identified mechanism of apoptosis regulation (No. 18 in Figure 1). The endoplasmic reticulum plays irreplaceable roles in protein folding, transport and secretion (Xu et al. 2005). ERS is triggered by intracellular homeostasis imbalance, and continuous ERS induces cells to enter the apoptotic program, which hampers cell function (Fernández et al. 2015). The main active ingredient of Dracaena cochinchinensis (Lour.) S. C. Chen (Liliaceae) is resina draconis (RD), which is extracted from the dried trunk of the plant. Studies have shown that RD can serve as an antioxidant and preservative compound (Choy et al. 2008). In a MI/R injury model (Yang et al. 2019), RD (1 mg/mL) has been found to effectively increase SOD activity and reduce MDA content almost to normal levels and significantly reduce the levels of GPR78, CHOP and other apoptosis-related proteins. These findings suggest that RD inhibits ER-induced apoptosis in MI/R injury by regulating miR-423-3p and its target ERK. For protecting the myocardium from reperfusion injury by targeting ERS, Allium fistulosum L. (Liliaceae) (Li 2019), Schisandra chinensis (Zhang et al. 2017) and Paeonia lactiflora (Zheng YP and Liu et al. 2019) are also available.