MOLECULES
·
2025
·Vol. 30
·期 7
·1481
·
IF 4.6
Wenhui Zhou,Boxu Dong,Ziqi Si,Yushuai Xu,Xinhua He,Ziyi Zhan,Yaru Zhang,Chaoyu Song,Zhuoqian Lv,Jiantao Zai,Xuefeng Qian
Sulfur hexafluoride (SF6), the strongest greenhouse gas, has great challenges in degradation because of its stable structure, posing significant environmental concerns. Photocatalysis offers an environmentally friendly, low-energy solution, but the fluoride deposition on catalysts reduces their activity, thus limiting their large-scale application. To prevent catalyst fluoride poisoning, we report a thin-layer graphitic carbon nitride (CN) material loaded with MoOx(CNM) that resists fluoride deposition for long-term SF6degradation. By combining molecular structure design and nanostructure regulation, we construct a photocatalyst with enhanced charge carrier mobility and reduced transport distances. We find that the CNM exhibits a high specific surface area, increased contact between reactants and active sites, and efficient electron–hole separation due to the Mo-N bonds, achieving an SF6degradation efficiency of 1.73 mmol/g after one day due to the prolonged catalytic durability of the catalyst, which is eight times higher than pristine g-C3N4(0.21 mmol/g). We demonstrate the potential of CNMs for low-energy, high-efficiency SF6degradation, offering a new approach to mitigate the environmental impact of this potent greenhouse gas. We envision that this study will inspire further research into advanced photocatalytic materials for environmental remediation, contributing to global efforts in combating climate change.
研究领域:
环境科学
·
材料科学
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产品关联
DOI
PubMed
高影响因子
CELL BIOCHEMISTRY AND BIOPHYSICS
·
2025
·
IF 2.5
Zhao Wenxin,Gong Zelin,Wang Benjie,Wu Zhiyu,Guo Yiyuan,Wang Shurong,Zhai Hao,Zheng Xiaomei,Yang Lu
Autophagy dysfunction plays an influential role in fluoride-induced neurotoxicity, but the mechanism has not yet been clarified. The aim of this study was to investigate the effects of grape seed proanthocyanidin extract (GSPE) on sodium fluoride (NaF)-treated offspring SD rats and SH-SY5Y cells, and to elucidate the mechanism of mTOR/p70s6k-mediated autophagy signaling pathway action. The results of in vivo experiments showed that different doses of GSPE treatment could alleviate NaF-induced neurological damage, centering on the improvement of learning and memory ability, recovery of autonomous exploration ability, reduction of anxiety-like behaviors, restoration of neuronal structure in hippocampal tissues, and reduction of the expression of apoptotic protein cleaved-PARP. Meanwhile, GSPE significantly promoted autophagy in hippocampal tissues, as evidenced by the blockage of mTOR/p70s6k phosphorylation and the upregulation of LC3-II and downregulation of p62 expression. To further explore the mechanistic issues, we conducted cellular experiments, which suggested that GSPE pretreatment significantly increased cell viability and strengthened autophagy compared with the NaF group. These results were evidenced by the inhibition of mTOR/p70s6k phosphorylation and the upregulation of LC3-II protein. To further investigate the effect of GSPE on the mTOR/p70s6k pathway, the mTOR inhibitor rapamycin (RAPA) and activator MHY1485 were incorporated. The results indicated that GSPE inhibited the enhancement of mTOR phosphorylation in combination with MHY1485, and further inhibited the phosphorylation of mTOR in combination with RAPA, and the levels of LC3-II and p62 and immunofluorescence results also confirmed that the pretreatment of GSPE promoted cellular autophagy. Similarly, Hoechst33342 fluorescence intensity and apoptotic protein cleaved-PARP expression were further reduced after GSPE combined with RAPA or MHY1485. In addition, downstream of the mTOR/p70s6k pathway, brain-derived neurotrophic factor (BDNF), which has been widely used in studies of mood disorders, was significantly reduced by GSPE pretreatment, suggesting that GSPE may not only have a role in attenuating neurotoxicity, but also potentially in improving mood. In conclusion, the present study reveals that GSPE may alleviate fluoride-induced neurotoxicity by inhibiting the activation of the mTOR/p70s6k signaling pathway and thereby enhancing cellular autophagy and antagonizing apoptosis.
研究领域:
神经毒理学
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分子生物学
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药理学
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发育神经科学
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细胞自噬
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环境健康
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产品关联
DOI
PubMed
高影响因子
NEUROCHEMICAL RESEARCH
·
2022
·Vol. 48
·期 2
·591-603
·
IF 4.414
Chen Rui,Xu Wan,Sun Yifu,Zhi Rongrong,Xie Peng,Zhi Zhongwen,Tang Xiaohong,Zhang Caiyi
2-(2-benzofu-ranyl)-2-imidazoline (2-BFI) is a drug that has attracted much attention in recent years. It has a therapeutic effect on brain diseases in animal models such as Alzheimer’s disease and cerebral infarction. However, whether 2-BFI affords neuroprotection against the toxicity of fluoride, which can cross the blood–brain barrier and cause neurological dysfunction is not known. We investigated the cell viability and apoptosis of SH-SY5Y cells and primary cultures of cortical neurons exposed to fluoride, and 2-BFI was used to protect both two kinds of cells against the effects of fluoride. We found that 2-BFI can provide neuroprotection on SH-SY5Y cells and primary cultures of cortical neurons upon fluorosis by maintaining the stability of endoplasmic reticulum–mitochondria contact sites and inhibiting activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome. This study may provide a new method for protecting against the neurotoxicity induced by fluoride exposure.
研究领域:
神经科学
·
药理学
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毒理学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2023
·
IF 8.9
Dongxu Wang,Kai Yin,Yue Zhang,Hongmin Lu,Lulu Hou,Hongjing Zhao,Mingwei Xing
Endemic fluorosis (EF) has been listed as one of the serious public health problems in many countries. Long-term exposure to high fluoride can lead to severe neuropathological damage to the brain. Although long-term research has revealed the mechanism of some brain inflammation caused by excessive fluoride, the role of intercellular interactions, especially immune cells, in brain damage is still unclear. Fluoride can induce ferroptosis and inflammation in the brain in our study. A co-culture system of neutrophil extranets and primary neuronal cells showed that fluoride can aggravate neuronal cell inflammation by causing neutrophil extranets (NETs). In terms of the mechanism of action, we found that fluoride leads to the opening of calcium ion channels by causing neutrophil calcium imbalance, which in turn leads to the opening of L-type calcium ion channels (LTCC). Extracellular free iron enters the cell from the open LTCC, leading to neutrophil ferroptosis, which releases NETs. Blocking LTCC (nifedipine) rescued neutrophil ferroptosis and reduced the generation of NETs. Inhibition of ferroptosis (Fer-1) did not block cellular calcium imbalance. In summary, our study explores the role of NETs in fluoride-induced brain inflammation and suggests that blocking calcium channels may be one of the possibilities to rescue fluoride-induced ferroptosis.
研究领域:
神经科学
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免疫学
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毒理学
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细胞生物学
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DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2023
·
IF 6.8
Wei-yu Guo,Ding-yan Lu,Zhi-zhong Guan,Lin Zheng,Shuai-shuai Chen,Ting Liu
To investigate the impact of the ethanoic fractions of Periploca forrestii Schltr. (P. forrestii) in ameliorating the liver injury caused by fluoride ingestion and to explore the potential mechanisms. Initially, an in vitro fluorosis cell model was constructed using the human normal liver cell line (L-02) induced by fluoride. Cell viability was assessed using the CCK-8 assay kit. The lactate dehydrogenase (LDH) assay kit was utilized to measure LDH content in the cell supernatant, while the malonic dialdehyde (MDA) assay kit was employed to determine MDA levels within the cells. Subsequently, a fluorosis rat model was established, and LDH content in the cell supernatant was measured using the LDH assay kit. Various parameters, including MDA, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and reactive oxygen species (ROS) content within the cells, were detected using appropriate assay kits. Additionally, cell apoptosis rate was determined using the Annexin V-FITC/PI cell apoptosis assay kit. The protein expression levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase-3, Cleaved Caspase-3, Caspase-9, and Cleaved Caspase-9 were analyzed through Western blotting. Compared to the model group, the ethanolic fraction D of P.forrestii (Fr.D) increased cell viability ( P < 0.01) and decreased LDH and MDA levels ( P < 0.01). In the high-dose Fr.D treatment group of fluoride-poisoned rats, serum ALT, AST, LDH and MDA levels significantly decreased ( P < 0.01). Results from rat primary cells exhibited that the Fr.D administration group exhibited significantly higher cell survival rates than the fluoride group ( P < 0.01). Similarly, primary rat cells treated with Fr.D showed enhanced cell viability ( P < 0.05) and reduced apoptosis rate, LDH, MDA, SOD, GSH-Px, CAT, and ROS levels ( P < 0.05) compared to the model group. Western blot analysis indicated that the Fr.D treatment group elevated the Bcl-2/Bax protein expression ratio and reduced Caspase-3 and Caspase-9 activation levels ( P < 0.01) compared to the model group. The results suggest that components within the Fr.D from Periploca forrestii may alleviate fluoride-induced liver injury by potentially counteracting oxidative stress and cell apoptosis.
研究领域:
药理学
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毒理学
·
细胞生物学
·
生物化学
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产品关联
DOI
PubMed
高影响因子
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