SCIENCE OF THE TOTAL ENVIRONMENT
·
2024
·
IF 8.2
Guang Tian,Falin He,Xiangxiang Li,Shaoyang Hu,Xingchen Zhao,Shuqi Guo,Tingting Wang,Hao Wang,Wansong Zong,Rutao Liu
Chromium (Cr) poses a high ecological risk, however the toxic mechanisms of Cr in different valence states to soil organisms at cellular and molecular levels are not exactly. In this study, the Eisenia fetida coelomocytes and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) were chosen as the target subjects to investigate the effects and mechanisms of cellular toxicity induced by Cr(VI) and Cr(III). Results indicated that Cr(VI) and Cr(III) significantly reduced the coelomocytes viability. The level of reactive oxygen species (ROS) was markedly increased after Cr(VI) exposure, which finally reduced antioxidant defense abilities, and induced lipid peroxidation and cellular membrane damage in earthworm coelomocytes. However, Cr(III) induced lower levels of oxidative stress and cellular damage with respect to Cr(VI). From a molecular perspective, the binding of both Cr(VI) and Cr(III) with Cu/Zn-SOD resulted in protein backbone loosening and reduced β-Sheet content. The Cu/Zn-SOD showed fluorescence enhancement with Cr(III), whereas Cr(VI) had no obvious effect. The activity of Cu/Zn-SOD continued to decrease with the exposure of Cr. Molecular docking indicated that Cr(III) interacted more readily with the active center of Cu/Zn-SOD. Our results illustrate that oxidative stress induced by Cr(VI) and Cr(III) plays an important role in the cytotoxic differences of Eisenia fetida coelomocytes and the binding of Cr with Cu/Zn-SOD can also affect the normal structures and functions of antioxidant defense-associated protein.
研究领域:
环境毒理学
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分子生物学
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生态毒理学
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DOI
PubMed
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
·
2025
·
IF 5.6
Die Hu,Xuexun Zhang,Shiwen Gong,Wentao Ma,Bo Cheng,Jing Yang,Lesan Yan,Binbin Li,Tong Qiu,Xinyu Wang
With the wide application of soft tissue fillers, implant material-induced inflammatory reactions have become a key factor affecting the therapeutic efficacy. This study developed an injectable filler with enhanced anti-inflammatory and antioxidant effects by adsorbing glycyl-L-histidyl-L-lysine copper complex (GHK-Cu) onto hydroxyapatite microspheres (HAPs), marking the first combination of HAPs and GHK-Cu to address inflammation caused by soft tissue fillers. GHK-Cu was successfully loaded onto HAPs by electrostatic adsorption. HAPs were then mixed with carboxymethyl cellulose (CMC), glycerol (GLY), and water to form GHK-Cu@CMHA gel. The study focus on the effective combination of HAPs as a carrier for sustained GHK-Cu delivery and the anti-inflammatory properties of GHK-Cu. GHK-Cu@CMHA exhibits sustained release properties for 7 days, which ensures prolonged therapeutic effects, minimizes peptide waste and reduces injection frequency, with good flowability and injectability. In the model of LPS-induced inflammation model in vivo and in vitro, GHK-Cu@CMHA gel reduced levels of inflammatory factors and Reactive oxygen species (ROS) levels decreased, while superoxide dismutase (SOD) activity was enhanced. In this process, H&E staining and Masson staining revealed significant collagen deposition. These findings further confirm that GHK-Cu@CMHA is a novel injectable soft tissue filler with good anti-inflammatory and antioxidant properties, which holds well potential for inflammation inhibition.
研究领域:
生物材料
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组织工程
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生物医学工程
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药剂学
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炎症研究
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纳米技术
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产品关联
DOI
PubMed
高影响因子
Small
·
2018
·Vol. 14
·期 13
·1703736
·
IF 9.598
Jun-Ying Wang,Xiaoyu Mu,Yonghui Li,Fujuan Xu,Wei Long,Jiang Yang,Peixian Bian,Junchi Chen,Lufei Ouyang,Haile Liu,Yaqi Jing,Jingya Wang,Lingfang Liu,Haitao Dai,Yuanming Sun,Changlong Liu,Xiao-Dong Zhang
Catalytic nanomaterials can be used extrinsically to combat diseases associated with a surplus of reactive oxygen species (ROS). Rational design of surface morphologies and appropriate doping can substantially improve the catalytic performances. In this work, a class of hollow polyvinyl pyrrolidone-protected PtPdRh nanocubes with enhanced catalytic activities for in vivo free radical scavenging is proposed. Compared with Pt and PtPd counterparts, ternary PtPdRh nanocubes show remarkable catalytic properties of decomposing H 2 O 2 via enhanced oxygen reduction reactions. Density functional theory calculation indicates that the bond of superoxide anions breaks for the energetically favorable status of oxygen atoms on the surface of PtPdRh. Viability of cells and survival rate of animal models under exposure of high-energy γ radiation are considerably enhanced by 94% and 50% respectively after treatment of PtPdRh nanocubes. The mechanistic investigations on superoxide dismutase (SOD) activity, malondialdehyde amount, and DNA damage repair demonstrate that hollow PtPdRh nanocubes act as catalase, peroxidase, and SOD analogs to efficiently scavenge ROS.
研究领域:
纳米材料
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催化
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生物医学工程
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辐射生物学
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材料科学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2021
·
IF 4.932
Xiaoqi Sun,Xiaotian Wang,Qianqian He,Muqing Zhang,Li Chu,Yang Zhao,Yongchao Wu,Jianping Zhang,Xue Han,Xi Chu,Zhonglin Wu,Shengjiang Guan
Baicalin (BA), a kind of flavonoids compound, comes from Scutellaria baicalensis Georgi (a kind of perennial herb) and has beneficial effects on the cardiovascular system through anti-oxidant, anti-inflammation, and anti-apoptosis actions. However, the therapeutic effects and latent mechanisms of BA on arsenic trioxide (ATO)-induced cardiac toxicity has not been reported. The present research was performed to explore the effects and mechanisms of BA on ATO-induced heart toxicity. Male Kunming mice were treated with ATO (7.5 mg/kg) to induce cardiac toxicity. After the mice received ATO, BA (50 and 100 mg/kg) was administered for estimating its cardioprotective effects. Statistical data demonstrated that BA treatment alleviated electrocardiogram abnormalities and pathological injury caused by ATO. BA could also lead to recovery of CK and LDH activities to normal range and cause a decrease in MDA levels and ROS generation, augmentation of SOD, CAT, and GSH activities. We also found that BA caused a reduction in the expression of proinflammatory cytokines, such as TNF-α and IL-6. Moreover, BA attenuated ATO-induced apoptosis by promoting the expression of Bcl-2 and suppressing the expression of Bax and caspase-3. TUNEL test result demonstrated BA caused impediment of ATO-induced apoptosis. Furthermore, BA treatment suppressed the high expression of TLR4 , NF-κB and P-NF-κB caused by ATO. In conclusion, these results indicate that BA may alleviate ATO-induced cardiac toxicity by restraining oxidative stress, apoptosis, and inflammation, and its mechanism would be associated with the inhibition of the TLR4/NF-κB signaling pathway.
研究领域:
药理学
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毒理学
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心脏病学
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DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
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2014
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IF 3.63
Demei Xu,Lihua Hu,Chuanyang Su,Xiaomin Xia,Pu Zhang,Juanli Fu,Wenchao Wang,Duo Xu,Hong Du,Qiuling Hu,Erqun Song,Yang Song
This study investigated the protective effects of curcumin on tetrachloro- p -benzoquinone (TCBQ)-induced hepatotoxicity in mice. TCBQ-treatment causes significant liver injury (the elevation of serum AST and ALT activities, histopathological changes in liver section including centrilobular necrosis and inflammatory cells), oxidative stress (the elevation of TBAR level and the inhibition of SOD and catalase activities) and inflammation (up-regulation of iNOS , COX-2, IL-1β, IL-6, TNF-α and NF-κB). However, these changes were alleviated upon pretreatment with curcumin. Interestingly, TCBQ has no effect on caspase family genes or B-cell lymphoma 2 (Bcl-2)/Bcl-2 associated X (Bax) protein expressions, which implied that TCBQ-induced hepatotoxicity is independent of apoptosis. Moreover, curcumin was shown to induce phase II detoxifying/antioxidant enzymes HO-1 and NQO1 through the activation of nuclear factor erythroid-derived 2-like 2 (Nrf2). In summary, the protective mechanisms of curcumin against TCBQ-induced hepatoxicity may be related to the attenuation of oxidative stress, along with the inhibition of inflammatory response via the activation of Nrf2 signaling.
研究领域:
药理学
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毒理学
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肝病学
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2019
·
IF 3.361
Chunyan Li,Xiao Sun,Ang Li,Min Mo,Zhongxi Zhao
Pulmonary fibrosis (PF) is a disease characterized by diffusing alveolar inflammation and alveolar structural disorders that ultimately lead to pulmonary interstitial fibrosis. S-allylmercaptocysteine (SAMC) as a water-soluble organosulfur garlic derivative exhibits efficient anti-inflammatory and anti-oxidative activities. In this study, we attempted to explore the function of SAMC in inhibiting bleomycin (BLM)-induced pulmonary fibrosis in mice. 0.035 U/g of BLM was intraperitoneally injected into mice twice per week for 4 weeks to induce fibrosis. SAMC (25 and 50 mg/kg) and N-acetylcysteine (NAC, 600 mg/kg) were given to mice for 28 days. The results indicate that SAMC could significantly ameliorate the pathological structure, and decrease inflammatory cell infiltration and pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) in BLM-induced pulmonary fibrosis mice. SAMC showed an anti-fibrosis effect by increasing anti-oxidants like HO-1, GSH and SOD as well as decreasing hydroxyproline (HYP) in BLM-induced mice. Mechanistic studies suggested that SAMC alleviated oxidative stress probably by impacting the Nox4/Nrf2 pathways, and played an anti-fibrosis role with decreasing the expression of α-SMA, collagen III, collagen I by suppressing the TGF-β1/Smad pathway. These findings indicate that SAMC may be partially responsible for the therapeutic effect on PF patients.
研究领域:
药理学
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肺科学
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免疫学
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病理学
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产品关联
DOI
PubMed
高影响因子
Journal of Advanced Research
·
2023
·
IF 10.7
Chenxiao Jiang,Qianzhi Shi,Jing Yang,Hao Ren,Lu Zhang,Shan Chen,Jiayi Si,Yihai Liu,Dujuan Sha,Biao Xu,Jie Ni
Introduction Sepsis-induced cardiac injury is the leading cause of death in patients. Recent studies have reported that reactive oxygen species (ROS)-mediated ferroptosis and macrophage-induced inflammation are the two main key roles in the process of cardiac injury. The combination of ferroptosis and inflammation inhibition is a feasible strategy in the treatment of sepsis-induced cardiac injury. Objectives In the present study, ceria nanozyme coordination with curcumin (CeCH) was designed by a self-assembled method with human serum albumin (HSA) to inhibit ferroptosis and inflammation of sepsis-induced cardiac injury. Methods and results The formed CeCH obtained the superoxide dismutase (SOD)-like and catalase (CAT)-like activities from ceria nanozyme to scavenge ROS, which showed a protective effect on cardiomyocytes in vitro . Furthermore, it also showed ferroptosis inhibition to reverse cell death from RSL3-induced cardiomyocytes, denoted from curcumin. Due to the combination therapy of ceria nanozyme and curcumin, the formed CeCH NPs could also promote M2 macrophage polarization to reduce inflammation in vitro . In the lipopolysaccharide (LPS)-induced sepsis model, the CeCH NPs could effectively inhibit ferroptosis, reverse inflammation, and reduce the release of pro-inflammatory factors, which markedly alleviated the myocardial injury and recover the cardiac function. Conclusion Overall, the simple self-assembled strategy with ceria nanozyme and curcumin showed a promising clinical application for sepsis-induced cardiac injury by inhibiting ferroptosis and inflammation.
研究领域:
纳米技术
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药理学
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心脏病学
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炎症研究
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氧化应激
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产品关联
DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2023
·
IF 5
Meng Chen,Qilan Hu,Shengquan Wang,Ling Tao,Xiaoxia Hu,Xiangchun Shen
Our previous data confirmed that 1,8-Cineole had an antihypertensive effect in animal models. However, it is unclear whether antihypertension is dependent on the protective effect of 1,8-Cineole on endothelial function and structure. At present, the purpose was to investigate the protective effects of 1,8-Cineole on vascular endothelial tissue in hypertensive rats and human umbilical vein endothelial cells (HUVECs). Our results showed that 1,8-Cineole significantly reduced the blood pressure and improved the vascular endothelial lesion , attenuated vascular oxidative stress and inflammation induced by Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) in rats. Pretreatment with 1,8-Cineole was able to inhibit the increase in malondialdehyde (MDA) and reactive oxygen species (ROS) induced by L-NAME, and increased the release and expression of superoxide dismutase (SOD) and nitric oxide (NO). In addition, 1,8-Cineole also reversed the increase of autophagy-associated protein LC3Ⅱ/LC3Ⅰ and the decrease of P62 in vivo and in vitro respectively. There was a synergistic effect between PI3K agonists and drugs, while PI3K inhibitors blocked the efficacy of 1,8-Cineole. The addition of autophagy inhibitor chloroquine increases the expression of eNOS. Taken together, our results indicate that 1,8-Cineole has potential beneficial promising antihypertension depending on the integrity of vascular endothelial structure and function induced by L-NAME, and the mechanism involves ameliorating autophagy by regulating of PI3K/mTOR.
研究领域:
药理学
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心血管疾病
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分子生物学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
American Journal of Translational Research
·
2020
·
IF 3.375
Jinwu Wang,Jie Cai,Xingyu Wang,Gaosheng Zhu,Yongzeng Feng,Hua Chen,Leyi Cai
Acute blunt skeletal muscle injury occurs frequently in sports and traffic accidents, and even leads to muscle necrosis and impaired functionality. Current treatment options for muscle injuries remain suboptimal and often result in delayed/incomplete recovery of damaged muscles. Tanshinone IIA is extracted from Salvia Miltiorrhizae, which is effective in the treatment of injury repair. But the clinical application of tanshinone IIA is limited due to its low water solubility, low permeability to biofilm and low bioavailability. In this study, tanshinone IIA liposomes were prepared to improve the bioavailability and sustained release of tanshinone IIA. The particle size, dispersion coefficient, zeta potential, encapsulation efficiency (EE) and drug loading (DL) of tanshinone IIA liposomes were 150.67 ± 27.23 nm, 0.20 ± 0.015, -8.73 ± 2.28 mV, 70.32 ± 4.04% and 15.63%, respectively. The results of quantitative real-time polymerase chain reaction (QRT-PCR) showed that tanshinone IIA liposome significantly promoted the expression of vimentin and reduce MHCIIB expression compared with other groups (P < 0.05). Western blotting showed that tanshinone IIA liposome could effectively promote the expression of autophagy-related proteins (VPS34, Beclin 1 and CTSD) and decrease p62 expression levels to treat injured muscle. Through HE, immunohistochemistry, ELISA and serological tests, we found that tanshinone IIA liposome not only effectively promoted the expression of desmin, but also reduced the expression of collagen-I and inhibited the production of pro-inflammatory factors, such as tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) (P < 0.05). In addition, tanshinone IIA liposome therapy significantly reduced the level of malondialdehyde (MDA) and increased the activity of superoxide dismutase (SOD) after muscle injury compared with other groups (P < 0.05). In conclusion, tanshinone IIA liposome possesses an effective therapeutic effect on acute blunt muscle injury in rats by augmenting autophagy and alleviating oxidative stress. The continuous release of tanshinone IIA encapsulated by liposomes for disease treatment provide a new idea for the efficient and safe use of drugs with low lipid solubility and bioavailability for the treatment of acute blunt muscle injury and repair of other injuries.
研究领域:
药理学
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生物技术
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肌肉骨骼系统
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药物递送系统
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损伤修复
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ACTA HISTOCHEMICA
·
2019
·
IF 1.719
Yang Wang,Chun Wang,Yue Zhang,Guan Wang,Haitao Yang
Sevoflurane is a widely used inhaled anesthetic , which triggers neuroapoptosis and oxidative damage in the developing central nervous system and cognitive dysfunction later in life. However, no effective therapeutic strategy for sevoflurane-induced deleterious effects is well developed. The purpose of the present study was to explore whether luteoline could attenuate neonatal sevoflurane exposure-triggered neurotoxicity . In this study, six-day-old C57BL/6 mice were pretreated with luteoline (30, 60 mg/kg) intraperitoneally for 30 min before exposed to 3% sevoflurane 6 h consecutively. We first examined the effects of luteoline on hippocampal neuron apoptosis, inflammation and oxidative stress 18 h post anesthesia. The spatial learning and memory performance was measured using Morris water maze test from postnatal day 31 to 38. The results showed that luteoline ameliorated neuronal apoptosis as evidenced by decrease of apoptotic cells, downregulation of the cleavage levels of caspase-3 and PRAP, and inactivation of caspase-3. Moreover, luteoline significantly decreased protein expressions of inflammatory cytokines (IL-1β, IL-18 and TNF-α), inhibited NF-кB/NLRP3 pathway (NF-кB, NLRP3 , ASC and caspase-1) and suppressed NF-кB activity. Our analyses indicated that luteoline had a significant effect on decreasing the contents of ROS and MDA , elevating the activity of SOD, and ultimately improving spatial learning and memory deficits of mice. In summary, our findings confirm that the attenuation of luteoline on sevoflurane-induced spatial learning and memory impairment later is associated with inhibition of hippocampal neuron apoptosis, inflammation and oxidative stress early. Luteoline might be a potential therapeutic for sevoflurane anesthesia-induced neurobehavioral dysfunction.
研究领域:
药理学
·
神经科学
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麻醉学
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产品关联
DOI
PubMed
高影响因子
APPLIED ORGANOMETALLIC CHEMISTRY
·
2022
·Vol. 36
·期 4
·e6587
·
IF 4.072
Dan Mo,Xun Song,Jiri Wu,Yogini Jaiswal,Yifu Guan,Yuzhen Zhang,Yunjun Shen,Hedong Bian
Metal complexes have been reported to possess excellent free radical scavenging and antimicrobial properties. In the present study, seven linear trinuclear complexes were synthesized based on bis Schiff base ligand and complexes 1 , 3 – 7 are reported for the first time. Their structure was characterized by IR spectroscopy and single crystal diffraction. BSA was used as carrier to hybridize the synthesized complexes to construct hybrid proteins. The interaction between metal complex and BSA was studied by UV–Vis spectrophotometry and fluorescence spectroscopy. Static quenching was the main mechanism identified for the interaction between metal complex and BSA. In the superoxide dismutase (SOD) activity test, IC 50 values of complexes and hybrid proteins range between 2.89 and 26.53 μM, with hybrid proteins demonstrating a stronger activity than the complexes. Among all the complexes studied, complex 5 exhibited the strongest inhibition against Candida albicans (MIC 12.5 μg ml −1 ) and Cryptococcus neoformans (MIC 6.5 μg ml −1 ).
研究领域:
无机化学
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生物化学
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药学
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微生物学
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产品关联
DOI
高影响因子
JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
·
2022
·
IF 5.062
Yawei Wang,Hongbing Lin,Xuetao Zhao,Tong Ding,Yuqin Shen
Periodontitis is a chronic inflammatory disease characterized by alveolar bone loss , which affects the integrity of the tissue supporting the teeth. Previous studies have shown that reactive oxygen species (ROS) can promote the secretion of inflammatory factors and cause alveolar bone inflammatory reactions and bone resorption. Therefore, scavenging ROS is important for reducing the expression of inflammatory factors and improving the inflammatory environment of alveolar bone tissue. Superoxide dismutase (SOD) is one of the most effective antioxidant enzymes for eliminating ROS, which can protect cells from ROS toxicity and reduce the level of intracellular oxidative stress and inflammation. However, SOD molecules have shortcomings, such as short half-life and insufficient stability, which limit the application of SOD in inhibiting periodontal bone resorption. The use of carrier zeolitic imidazolate framework-90 (ZIF-90) with ATP-responsiveness and good biocompatibility can protect SOD molecules, improve SOD stability, and achieve intracellular SOD delivery. Therefore, we fixed SOD into ZIF-90 using the co-precipitation method to prepare ATP-responsive [email protected] and designed a study to investigate the ability of ATP-responsive [email protected] to reduce the inflammatory response of lipopolysaccharide (LPS)-stimulated human osteoblast MG-63. In our study, the ATP-responsive assembly efficiently suppressed the levels of ROS and pro-inflammatory cytokines, showing great potential to ameliorate the levels of oxidative stress, reduce inflammation, and increase osteoblast activity. This provides a novel idea for the application of SOD in alveolar bone resorption.
研究领域:
药学
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生物材料
·
口腔科学
·
细胞生物学
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产品关联
DOI
高影响因子
危险品化学品经营许可证（带存储）