Aluminum trichloride caused hippocampal neural cells death and subsequent depression-like behavior in rats via the activation of IL-1β/JNK signaling pathway

Zhang, Haiyang; Wei, Mian; Lu, Xiangyu; Sun, Qingping; Wang, Chuqiao; Zhang, Jiuyan; Fan, Honggang

doi:10.1016/j.scitotenv.2020.136942

Cited by 39 publications

(22 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous experiments in our laboratory have demonstrated that Se deficiency damages myocardial cells via the necroptosis pathway (Yang et al, 2018), and recent comments have suggested that Se status is inversely related to the severity of IBD (Kudva et al, 2015). TNF‐α‐induced death receptor signaling promotes necroptosis in many different target cell types (Vercammen, Vandenabeele, Beyaert, Declercq, & Fiers, 1997; H. Zhang et al, 2020). Consistent with previous studies, we found that Se deficiency could cause a significant increase in the mRNA and protein expression of IPEC‐J2 cells through the TNF‐α necroptosis pathway.…”

Section: Discussionmentioning

confidence: 99%

Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Zhang

Bao

et al. 2020

Journal Cellular Physiology

View full text Add to dashboard Cite

Selenium (Se) deficiency has a significant impact on the swine breeding industry by inducing digestive system damage and diarrhea. However, the molecular mechanism remains unclear. Our objectives were to investigate if different amounts of necroptosis, inflammatory responses, and T helper cell 1/T helper cell 2 (Th1/Th2) imbalances were induced by Se deficiency in intestinal porcine jejunal epithelial cells (IPEC-J2) and swine ileum tissue. Therefore, Se-deficient models were successfully established both in vitro and in vivo. In the current study, the cell morphological observation results showed that Se deficiency seriously affected the growth and differentiation of IPEC-J2 cells. Moreover, the necroptosis staining and histomorphology observation results showed that the number of necroptotic cells increased significantly, and the ileal tissue exhibited abnormal structures, including necroptotic features and inflammatory cell infiltration, in the Se-deficient group. Furthermore, Se deficiency resulted in accelerated cell necroptosis by increasing (p < .05) the expression of genes related to the tumor necrosis factor-α pathway at both the protein and messenger RNA (mRNA) levels compared to the control group. Moreover, the relative mRNA and protein expression of the inflammatory genes and their responses to dietary Se deficiency were consistent with the resultant Th1/Th2 imbalances in vitro and in vivo. Taken together, the results suggested that Se deficiency caused necroptosis, inflammatory responses, and abnormal expression of cytokines in swine ileum tissue. These findings might help us to explain the damage induced by Se deficiency to the digestive system of swine.

show abstract

Section: Discussionmentioning

confidence: 99%

Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Zhang

Bao

et al. 2020

Journal Cellular Physiology

View full text Add to dashboard Cite

show abstract

“…Exposure to Al was also shown to reduce circulating serotonin levels (Zhang et al, 2016a,b,c). Interestingly, however, a recent study concludes that Al-induced depressive-like behavior in rats is due to activation of hippocampal IL-1β/JNK signaling pathway, resulting in neuronal death in this region (Zhang et al, 2020).…”

Section: Serotoninergic Systemmentioning

confidence: 96%

“…This observation corresponds to the proposed role of necroptosis in Al neurotoxicity (Zhang, 2018a,b). The latter was observed at high doses (450 mg/ kg AlCl 3 ), whereas lower doses more likely induced apoptosis through IL-1β/JNK signaling pathway (Zhang et al, 2020). Another study also demonstrated that Al-induced apoptosis and necrosis differentially involved ERK and p38 MAPK/ERK signaling pathways in SH-SY5Y cells, respectively (Jia et al, 2014).…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 96%

Molecular mechanisms of aluminum neurotoxicity: Update on adverse effects and therapeutic strategies

Skalny

Aschner

Jiang

et al. 2021

Advances in Neurotoxicology

View full text Add to dashboard Cite

HAL is a multi-disciplinary open access archive for the deposit and dissemination of scientific research documents, whether they are published or not. The documents may come from teaching and research institutions in France or abroad, or from public or private research centers. L'archive ouverte pluridisciplinaire HAL, est destinée au dépôt et à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.

show abstract

“…The open field test was conducted to test locomotor activity [38]. Briefly, mice were placed in a square arena (30 cm × 30 cm × 30 cm) with clear Plexiglas walls and dim illumination.…”

Section: Open Field Testmentioning

confidence: 99%

Ellagic acid protects mice against sleep deprivation-induced memory impairment and anxiety by inhibiting TLR4 and activating Nrf2

Wang

Yang

Liu

et al. 2020

Aging

View full text Add to dashboard Cite

Sleep disorder has become a prevalent issue in current society and is connected with the deterioration of neurobehaviors such as mood, cognition and memory. Ellagic acid (EA) is a phenolic phytoconstituent extracted from grains and fruits that has potent neuroprotective properties. This research aimed to study the alleviative effect and mechanism of EA on memory impairment and anxiety caused by sleep deprivation (SD). EA ameliorated behavioral abnormalities in SD mice, associated with increased dendritic spine density, and reduced shrinkage and loss of hippocampal neurons. EA reduced the inflammatory response and oxidative stress injury caused by SD, which may be related to activation of the Nrf2/HO-1 pathway and mitigation of the TLR4-induced inflammatory response. In addition, EA significantly reduced the mortality and ROS levels in glutamate (Glu)-induced hippocampal neuron injury, and these effects of EA were enhanced in TLR4 siRNA-transfected neurons. However, knockdown of Nrf2 dramatically restrained the protective impact of EA on Glu-induced toxicity. Taken together, EA alleviated memory impairment and anxiety in sleep-deprived mice potentially by inhibiting TLR4 and activating Nrf2. Our findings suggested that EA may be a promising nutraceutical ingredient to prevent cognitive impairment and anxiety caused by sleep loss.

show abstract

Aluminum trichloride caused hippocampal neural cells death and subsequent depression-like behavior in rats via the activation of IL-1β/JNK signaling pathway

Cited by 39 publications

References 47 publications

Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Molecular mechanisms of aluminum neurotoxicity: Update on adverse effects and therapeutic strategies

Ellagic acid protects mice against sleep deprivation-induced memory impairment and anxiety by inhibiting TLR4 and activating Nrf2

Contact Info

Product

Resources

About