ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
·
2023
·
IF 5.8
Mu Yi,Che Bangwei,Tang Kaifa,Zhang Wenjun,Xu Shenghan,Li Wei,He Jun,Liu Miao,Chen Peng,Zhong Siwen,Li Guangyu
Polysaccharides from Dendrobium officinale polysaccharides ( DOP s) are the main bioactive components of Dendrobium officinale , which have the functions of antioxidation and immune regulation. However, it is not clear whether DOPs have any effect on the prevention of reproductive disorders induced by oxidative stress. The purpose of this study was to explore the protective effect of DOPs on reproductive oxidative stress injury in male mice and its possible mechanism. In this study, the mouse model of reproductive injury was established by intraperitoneal injection of cyclophosphamide (CTX). The reproductive function was evaluated by relative testicular mass, sperm parameters, and sex hormone levels. The oxidative stress level of male mice with reproductive injury treated with DOPs was analyzed by the levels of 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA), and nitric oxide (NO) in sperm. The expression of follicle-stimulating hormone receptor ( FSHR ) mRNA, androgen-binding ( ABP ) mRNA, and c-kit mRNA was detected by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) to explore its mechanism. After CTX administration, the sperm density, sperm motility, normal sperm morphology, and sex hormone levels in mice were significantly lower than those in the control group ( P < 0.05). At the same time, the expression of p53 protein was upregulated, and the expression of Bcl-2 protein was downregulated ( P < 0.05). In addition, the expression of FSHR and ABP mRNA on Sertoli cells was also significantly inhibited ( P < 0.05). DOPs can effectively reduce the oxidative stress injury of testicular tissue. After DOP treatment, the sperm quality and sex-related hormone levels of mice were significantly improved and positively correlated with the dose of DOPs ( P < 0.05). Administration of DOPs can reduce the damage caused by oxidative stress by reducing the level of oxidative stress, improving the hormone environment in testes, and regulating the expression of specific genes in Sertoli cells and spermatogenic cells.
研究领域:
药理学
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生殖生物学
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氧化应激
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2025
·
IF 5.4
Yan-Ling Qian,Bang-Yin Tan,Shi-Shi Qin,Xian-Run Wu,Zhuo-Qi Shi,Yun-Li Zhao,Xiao-Dong Luo
Ethnopharmacological relevance Crotalari a assamica Benth, one of the folk medicinal plants in the "Dai" of China, is commonly used to treat liver and bile related diseases. However, its bioactive compounds and the mechanism related to traditional use remain unclear. Aim of the study To investigate the protective compounds and mechanism of C . assamica on drug-induced liver injury. Materials and methods The acetaminophen (APAP)-induced mice and cell model were carried out to reveal the liver protection of the extract of C . assamica (ECA) and bioactive compounds in vitro and in vivo . The protective pathway was explored using transcriptome analysis, and binding targets were predicted by structure-based binding prediction and dynamic simulation, which were further supported by qPCR and Western Blot experiments on the livers of treated mice. Results ECA reduced the contents of serum lactate dehydrogenase, aspartate transaminase, and alanine transaminase significantly, adjusted the oxidative indices of serum and liver tissues, and ameliorated inflammation and necrosis of liver tissues, as well as up-regulated expressions of NQO1, HO-1, Nrf2, p-AKT, BCL-2, AKT, and IL-6 in vivo . Moreover, its bioactive compound sarosiensin V increased the viability of APAP-induced HepG2 cells, and restored liver function activity, accompanied by enhanced antioxidation and mitochondrial membrane potential significantly. Conclusion C. assamica and its bioactive compound sarosiensin V inhibited oxidative stress, inflammation, apoptosis and necrosis of liver tissues, which was associated with the upregulation of the Nrf2 pathway, and then supporting its traditional use for liver protection.
研究领域:
药理学
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肝脏病学
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分子生物学
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天然产物化学
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氧化应激
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药物代谢
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Oceanology and Limnology
·
2024
·Vol. 42
·期 1
·163-173
·
IF 1.3
Ma Dandan,Zhou Qingli,Sui Liying,Guo Qingbin,Liu Huanhuan,Liang Honghe,Li Zhenjing,Sang Zhongna
Deltamethrin (DEL), a commonly used pyrethroid pesticide, results in higher reactive oxygen species (ROS) levels in aquatic animals, which consequently unbalance the redox state. Phlorizin (PHL) is a flavonoid and a natural product promising to prevent or reduce pesticide-induced oxidative stress. Artemia is a micro-crustacean widely used in marine hatcheries and an experimental aquatic organism for environmental toxicology research. This research aimed to evaluate the toxicity of DEL on Artemia and the antioxidative effect of PHL against the toxicity. Results show that 0.08-mg/mL PHL exerted its antioxidative effects on hatching percentage of the cysts in 24-h incubation and on body length and survival rate of Artemia in 12-d culture. After 12-d culture, 12-, 24-, and 36-h DEL exposure showed significant drops in SOD, CAT, and GSH-Px enzyme activities, and significant increases in ROS and malondialdehyde (MDA) levels in Artemia ( P <0.05). On the contrary, 0.08-mg/mL PHL application improved the enzyme activities and decreased the ROS and MDA levels ( P <0.05). Moreover, 0.08-mg/mL PHL significantly increased mRNA expression levels of Cu/Zn SOD, CAT, GST, HO-1, NQO1 , and Nrf2 , and decreased mRNA expression level of Keap1 in the DEL-exposed Artemia ( P <0.05). Therefore, DEL is toxic to Artemia , while PHL alleviates DEL-induced oxidative damage by possibly regulating the Nrf2 signaling pathway. This study provided a theoretical basis for PHL to reduce pesticide-induced toxicity in aquatic animals.
研究领域:
环境毒理学
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水产动物健康
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抗氧化研究
✓ 已验证
DOI
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2023
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IF 6.8
Yang Xu,Yuting Gui,Dan Zhi,Jie Pi,Xinhua Liu,Jianguo Xiang,Deliang Li,Junhua Li
Cadmium (Cd) is one of the dominant metal pollutants present in the aquatic environment that affects ion homeostasis, oxidative stress (OS) and immune responses of aquatic organisms. Given the physicochemical similarities between Cd 2+ and calcium (Ca 2+ ) ions, their antagonism may facilitate the mitigation of Cd-induced toxicity. To better understand the role of Ca in protecting against Cd-induced toxicity in teleosts, juvenile grass carp were exposed to Cd (measured concentration 3 μg/L) and a gradient of Ca concentrations (measured concentration 1.5 mg/L, 2.5 mg/L, 3.0 mg/L, and 3.5 mg/L in the control (CTL) group, low calcium (LCA) group, medium calcium (MCA) group, and high calcium (HCA) group, respectively) for 30 days. Inductively coupled plasma mass spectrometry (ICP-MS) data analyses showed that simultaneous exposure to Ca impaired the accumulation of Cd in all tested tissues. Besides, Ca addition maintained the plasma ion (Na + , K + , Cl - ) homeostasis, alleviated Cd-induced oxidative stress (OS), and regulated the activities and transcriptional levels of ATPase. Furthermore, transcriptional heatmap analysis demonstrated that several indicator genes for OS and calcium signaling pathway were found to be significantly modulated by Ca addition. This work delineates a protective effect of Ca against Cd-induced toxicity in grass carp, providing new insight into the possible solutions to Cd pollution issues in aquaculture industry.
研究领域:
环境科学
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水产养殖学
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毒理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY
·
2024
·
IF 4.3
Zhong Wang,Wanting Li,Xiaomin Hou
As the most universally used anionic surfactant, ubiquitous existence and accumulation of sodium dodecyl benzene sulfonate (SDBS) in the environment has inevitably imposed the associated harmful impacts to plants due to producing excessive reactive oxygen species. However, the underlying hazardous mechanism of the SDBS-induced oxidative stress to plants at molecular level has never been reported. Here, the molecular interaction of AtPrxQ with SDBS was explored for the first time. The intrinsic fluorescence of AtPrxQ was quenched based on static quenching, and a single binding site of AtPrxQ towards SDBS and the potential interaction forces driven by hydrophobic interactions were predicted from thermodynamic parameters and molecular docking results. Besides, the interaction pattern of AtPrxQ and SDBS was also confirmed by the bio-layer interferometry with moderate binding affinity. Moreover, the structural changes of AtPrxQ along with the destructions of the protein framework and the hydrophobic enhancement around aromatic amino acids were observed upon binding with SDBS. At last, the toxic effects produced by SDBS on peroxidase activities and Arabidopsis seedlings growth were also characterized. Thus this work may provide insights on the molecular interactions of AtPrxQ with SDBS and assessments on the biological hazards of SDBS to plants even for the agriculture.
研究领域:
植物学
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环境毒理学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2020
·
IF 4.872
Tingting Liu,Tongtong Li,Lingyan Zhang,Haolin Li,Shangke Liu,Song Yang,Quanshun An,Canping Pan,Nan Zou
Salicylic acid (SA) is an important signal molecule, regulating oxidative stress response in plants. In this study, we evaluated the influences of SA (1 mg L −1 , 10 mg L −1 and 50 mg L −1 ) on the accumulation of clothianidin (CLO), dinotefuran (DFN) and difenoconazole (DFZ) (5 mg L −1 ) and pesticide-induced (CLO-10 mg L −1 , DFN-20 mg L −1 , and DFZ-10 mg L −1 ) oxidative stress in cucumber plants. Exogenous SA at 10 mg L −1 significantly reduced the half-lives of three pesticides in nutrient solution and prevented the accumulation of pesticides in roots and leaves. And the role of SA in reducing residues was related to the major accumulation sites of pesticides. By calculating the root concentration factor (RCF) and translocation factor (TF), we found that SA at 10 mg L −1 reduced the ability of roots to absorb pesticides and enhanced the translocation ability from roots to leaves. Roots exposed to high concentrations of three pesticides could reduce biomass, low chlorophyll content, increase the accumulation of reactive oxygen species (ROS) and proline, promote lipid peroxidation, and alter the activities of a range of antioxidant enzymes, respectively. Exogenous SA at low concentrations (1 mg L −1 and 10 mg L −1 ) significantly mitigated these negative effects. Hence, application of exogenous SA at 10 mg L −1 could effectively alleviate the accumulation of pesticides and induce stress tolerance in cucumber planting systems.
研究领域:
植物学
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环境科学
·
农业科学
✓ 已验证
DOI
PubMed
高影响因子
WATER AIR AND SOIL POLLUTION
·
2021
·Vol. 232
·期 9
·1-21
·
IF 2.52
Cano-Viveros Selene,Galar-Martínez Marcela,Gasca-Pérez Eloy,García-Medina Sandra,Ruiz-Lara Karina,Gómez-Oliván Leobardo Manuel,Islas-Flores Hariz
Aluminum, mercury, and iron have been found in high concentrations in various freshwater bodies around the world and have been shown to be very harmful contaminants to hydrobionts, causing metabolic dysfunction and damage at various levels. However, studies on mixtures of these pollutants are scarce, particularly in younger or developing organisms, which are more sensitive to damage. Therefore, the objective of this work was to evaluate the toxicity of Al, Fe, and Hg, in isolation and in mixture, on common carp embryos exposed to the maximum permissible limits described in the Mexican regulations for the protection of aquatic life, correlating the biomarkers of oxidative stress with the effects on embryonic development. For this purpose, the Cyprinus carpio embryos were exposed to iron (0.1 mg L −1 ), mercury (0.00001 mg L −1 ), aluminum (0.05 mg L −1 ), and their mixture, throughout their development and until hatching. The activity of the antioxidant enzymes (SOD, CAT, and GPx), the degree of lipoperoxidation, and the content of hydroperoxides and total proteins, as well as the morphological development of the embryos were evaluated at 12 h, 24 h, 48 h, 72 h, and 96 h of exposure. The results showed that the metals under study are toxic to C. carpio embryos and that their interaction modifies the toxic response. Thus, iron generates alterations in the activity of antioxidant enzymes and modification in embryonic development to a lesser extent than aluminum and the mixture of metals, while mercury exerts its toxicity on embryos by mechanisms other than oxidative stress, but the modification to the activity of antioxidant enzymes may contribute to the changes observed in embryonic development. The changes in the response of biomarkers of embryotoxicity and oxidative stress suggest that the combination of metals produces an antagonism-type interaction, so this study provides a precedent for future research to determine the type of interaction that a mixture of contaminants generates in developing aquatic organisms. Graphical abstract
研究领域:
环境毒理学
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水产生物学
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生态学
✓ 已验证
DOI
高影响因子
Nutrients
·
2023
·Vol. 15
·期 6
·1340
·
IF 5.9
Yu Li,Bo He,Chao Zhang,Yanji He,Tianyang Xia,Chunyu Zeng
Cardiac hypertrophy is accompanied by increased myocardial oxidative stress, and whether naringenin, a natural antioxidant, is effective in the therapy of cardiac hypertrophy remains unknown. In the present study, different dosage regimens (25, 50, and 100 mg/kg/d for three weeks) of naringenin (NAR) were orally gavaged in an isoprenaline (ISO) (7.5mg/kg)-induced cardiac hypertrophic C57BL/6J mouse model. The administration of ISO led to significant cardiac hypertrophy, which was alleviated by pretreatment with naringenin in both in vivo and in vitro experiments. Naringenin inhibited ISO-induced oxidative stress, as demonstrated by the increased SOD activity, decreased MDA level and NOX2 expression, and inhibited MAPK signaling. Meanwhile, after the pretreatment with compound C (a selective AMPK inhibitor), the anti-hypertrophic and anti-oxidative stress effects of naringenin were blocked, suggesting the protective effect of naringenin on cardiac hypertrophy. Our present study indicated that naringenin attenuated ISO-induced cardiac hypertrophy by regulating the AMPK/NOX2/MAPK signaling pathway.Keywords:naringenin;cardiac hypertrophy;oxidative stress;AMPK;NOX2
研究领域:
药理学
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心脏病学
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Toxicologic Pathology
·
2016
·
IF 0.848
Yuan Yuan,Shixun Ma,Yongmei Qi,Xue Wei,Hui Cai,Li Dong,Yufeng Lu,Yupeng Zhang,Qingjin Guo
The objective of the current study was to explore the inhibitory effects of quercetin on cadmium-induced autophagy in mouse kidneys. Mice were intraperitoneally injected with cadmium and quercetin once daily for 3 days. The LC3-II/β-actin ratio was used as the autophagy marker, and autophagy was observed by transmission electron microscopy. Oxidative stress was investigated in terms of reactive oxygen species, total antioxidant capacity, and malondialdehyde. Cadmium significantly induced typical autophagosome formation, increased the LC3-II/β-actin ratio, reactive oxygen species level, and malondialdehyde content, and decreased total antioxidant capacity. Interestingly, quercetin markedly decreased the cadmium-induced LC3-II/β-actin ratio, reactive oxygen species levels, and malondialdehyde content, and simultaneously increased total antioxidant capacity. Cadmium can inhibit total antioxidant capacity, produce a large amount of reactive oxygen species, lead to oxidative stress, and promote lipid peroxidation, eventually inducing autophagy in mouse kidneys. Quercetin could inhibit cadmium-induced autophagy via inhibition of oxidative stress. This study may provide a theoretical basis for the treatment of cadmium injury.
研究领域:
毒理学
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药理学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
MOLECULAR BIOLOGY REPORTS
·
2025
·Vol. 52
·期 1
·1-13
·
IF 2.8
Wu Wanqi,Wang Jun,Wang Guanglu,Wang Feibiao,Yang Yue,Liu Zhijun,Song Qimei,Chen Si,Chen Huizhen
Background Sepsis can cause severe cardiac damage, and matrix metalloproteinase 9 (MMP9) is involved in the inflammatory response and tissue injury processes. Monotropein is a monoterpene glycoside with anti-inflammatory and antioxidant effects. This study aims to investigate whether monotropein can alleviate sepsis-induced cardiac injury by affecting the activity of MMP9. Methods and results The correlation between MMP9 and septic cardiac injury was explored using differential expression gene analysis from the GEO database and an in vitro lipopolysaccharide (LPS)-stimulated H9c2 cell model. In a cecal ligation and puncture (CLP)-induced mouse sepsis model, the effects of monotropein on myocardial cell apoptosis, inflammatory factor expression, and antioxidant enzyme levels were validated through drug administration. The results showed that MMP9 was significantly upregulated in sepsis patients. In the H9c2 cell model, LPS-induced MMP9 activity was positively correlated with cell damage. Inhibition of MMP9 alleviates LPS-induced myocardial matrix disruption and apoptosis. Monotropein exerts anti-matrix degradation and anti-apoptotic effects through MMP9 in LPS-induced H9c2 cells. Monotropein also reduced the expression of LPS-induced inflammatory factors (TNF-α, IL-1β, IL-6).In the mouse model, monotropein decreased oxidative stress damage (lower MDA levels, increased GSH, T-AOC, CAT enzyme activity), and improved cardiac injury by inhibiting myocardial cell apoptosis-related proteins (Bax, Bcl-2, and Caspase-3 activation). Conclusion Monotropein exerts a protective effect on septic cardiac injury by inhibiting MMP9 activity, reducing inflammatory response, and enhancing antioxidant capacity, thereby ameliorating myocardial cell damage and apoptosis. Graphical abstract
研究领域:
医学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CELL DEATH AND DIFFERENTIATION
·
2025
·
IF 15.4
Chen Zixiang,Niu Kaifeng,Li Mengge,Deng Yuchun,Zhang Ji,Wei Di,Wang Jiaqi,Zhao Yongliang
Tumor cells evolve strong antioxidant capacities to counteract the abnormal high level of reactive oxygen species (ROS) in the tumor microenvironment. Glutamate-cysteine ligase catalyzing subunit (GCLC) for synthesis of antioxidant glutathione (GSH) represents the key enzyme to maintain redox homeostasis of tumor cells, however, whether its activity is regulated by posttranslational modifications, such as succinylation, remains to be clarified. Here, we demonstrate the existence of succinylation modification on GCLC by in vitro and in vivo assays. NAD-dependent deacetylase Sirtuin-2 (SIRT2) serves as the desuccinylase and catalyzes GCLC desuccinylation at sites of K38, K126, and K326. Specifically, GCLC directly interacts with SIRT2, which can be substantially enhanced upon ROS treatment. This strengthened association results in GCLC desuccinylation and activation, consequently promoting GSH synthesis and rendering cancer cells resistant to ferroptosis induction. Depletion of SIRT2 decreases total GSH level and meanwhile increases the cellular susceptibility to ferroptosis, which can mostly be rescued by introducing wild-type GCLC, but not its 3K-E mutant. We further demonstrated that histone acetyltransferase P300 serves as the succinyltransferase of GCLC, and their association is remarkably decreased after ROS treatment. Thus, SIRT2-regulated GCLC succinylation represents an essential signaling axis for cancer cells to maintain their redox balance in coping with oxidative stress-induced ferroptosis.
研究领域:
肿瘤生物学
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细胞代谢
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表观遗传学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BRAIN BEHAVIOR AND IMMUNITY
·
2025
·
IF 7.6
Xiaoyu Yu,Tingting Yang,Di Wu,Chenxue Xu,Zhuoran Li,Ao Sun,Shulei Gao,Heng Li,Zhenyu Fan,Rongrong Huang
Microglial inflammation has been implicated in the pathophysiology of major depressive disorder; however, the underlying biological mechanisms remain inadequately understood. Consequently, we conducted a screening of the Poly ADP-ribose (PAR) polymerase (PARP) family expression in the hippocampus of chronic unpredictable stress (CUS) mouse models and investigated the specific role of PARP14 in microglial inflammation and its association with depression. Here, this study demonstrated the elevated PARP14 expression in the hippocampus of CUS mice. The knockdown of PARP14 in the hippocampus did not mitigate depressive-like behaviors in mice, whereas overexpression of PARP14 significantly mitigated these behaviors. Furthermore, PARP14 was abundant in microglia, and microglial-targeted PARP14 overexpression significantly alleviated depressive-behaviors in CUS, reduced microglial activation, and inhibited the central inflammatory responses. Mechanistically, PARP14 positively regulated nicotinamide nucleotide transhydrogenase (NNT) expression in microglia, and the inflammatory response of microglia induced by PARP14 knockdown was suppressed through NNT overexpression. Additionally, deficiency in NNT led to an accumulation of reactive oxygen species (ROS) and subsequent microglial inflammation, which was effectively inhibited by the ROS inhibitor N-Acetylcysteine. These findings suggest that PARP14 alleviates depressive-like behaviors in mice by inhibiting microglial activation via NTT-mediated clearance of ROS.
研究领域:
神经科学
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免疫学
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药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）