SCIENCE OF THE TOTAL ENVIRONMENT
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2022
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IF 10.753
Xiaoping Liao,Jinru Cao,Meng Lei,Caixiang Zhang,Lisong Hu
Manganese sulfide ( MnS ) has unique reactive abilities and can affect the fate and toxicity of contaminants in the natural environment, specifically sulfidic sediments that undergo biogeochemical changes due to natural and artificial processes. However, the effect of oxidization induced by the oxygenation of MnS on organic contaminants remains poorly understood. Herein, we revealed that the hydroxyl radical ( HO ·) was the dominant reactive oxidant for the rapid degradation of the assessed hydrophobic organic contaminants (including azo dye, nitroaromatic compounds, pesticide, and an endocrine disrupt chemical) during the oxygenation of MnS based on the competitive dynamic experiments, quenching experiments and electron spin resonance (ESR) methods. The removal rates of the assessed organic contaminants were significantly dependent on MnS dosage and co-solutes, including sediment humic acid , metal ions ( Mn 2+ and Fe 3+ ), and inorganic anions ( PO 4 3− and Cl − ). HO · scavenging by sulfide and its oxidation products (e.g., elemental sulfur), rather than dissolved Mn 2+ , was responsible for the low utilization efficiency of HO · for the assessed contaminants. The contribution of the manganese oxide ( MnO 2 ) generated by the oxygenation of MnS to the examined degradation of contaminants could be neglected. Considered collectively, the reaction between H 2 O 2 and MnO 2 generated superoxide radicals ( O 2 − ·) which dominated the generation of HO · in an oxic MnS suspension. The results suggest that the impact of oxidization induced by the oxygenation of MnS on environmental contaminants should be of concern in both natural and engineered systems.
研究领域:
环境科学
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化学
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JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Xiaolin Xie,Haikang Fu,Zhixuan Ai,Ziwei Huang,Wenwen Tan,Qingfeng Xie,Yuhong Liu,Yucui Li,Jiannan Chen,Xiaobo Yang,Ziren Su,Zhengquan Lai,Jianhui Xie
Ethnopharmacological relevance Coptidis Rhizome (CR), a cornerstone medicinal herb, is routinely used to treat metabolic diseases for centuries in China. However, the potential mechanism has not been completely elucidated. Preceding investigation has reported that berberine in CR can bind to hemoglobin (Hb) and utilize erythrocyte-Hb self-assembly drug delivery system to significantly upregulate HO-1 expression. Aim of the study This study was designed in a pioneering endeavor to explore the therapeutic potential and underlying mechanism of CR in dexamethasone- and fructose-induced glycolipid metabolism disorders (GLD) rat models. Material and methods The major elements of CR were identified by high performance liquid chromatograph (HPLC). Dexamethasone- and fructose-induced rat GLD model was constructed. Glucolipid metabolism, oxidative status, and insulin sensitivity were investigated. Histopathological, transcriptomic, in silico simulations, immunofluorescence, immunohistochemistry, and Western blotting analyses were performed to gain further mechanism insight. Results HPLC analysis revealed that berberine, palmatine, coptisine, epiberberine, and jatrorrhizine were detected in CR, with berberine as the most abundant. Administration of CR favorably regulated the organ indexes, and significantly improved glucose metabolism by decreasing the FBG and GSP levels along with improved OGTT. CR promoted insulin sensitivity by suppressing the increased levels of FINS, HOMA-IR and ISI, and concomitantly improving ITT. Furthermore, CR normalized lipid metabolism by decreasing the elevated TG, TC and LDL-C levels. Additionally, CR effectively ameliorated histopathological deterioration in pancreatic and hepatic tissues and reduced serum ALT and AST activities. CR also ameliorated oxidative stress by remarkably lowering hepatic ROS fluorescence intensity and serum MDA content, whereas enhancing SOD and CAT enzymatic activity, and T-AOC level. Hepatic transcriptomics analysis revealed the oxidative stress-related gene HMOX1 encoding HO-1 and AMPK pathway critically involved in the therapeutic effect of CR. Furthermore, CR was found to significantly up-regulate the protein expression levels of HO-1, NQO1 and p-AMPK. On the other hand, in silico simulations indicated that strong van der Waals forces interaction between these alkaloids and HO-1. Notably, CR exhibited potent HO-1 agonistic activity comparable to the HO-1 inducer hemin, as manifested by enhanced HMOX1 mRNA level, HO-1 expression level, cytoplasmic HO-1 fluorescence intensity, carbon monoxide production, and reduced heme level, which were the markers of erythrocyte metabolism. Administration of CR or hemin significantly improved fasting glycemia, blood fat, insulin sensitivity, and antioxidant capacity. Nevertheless, these effects were observably reversed by the HO-1 inhibitor zinc protoporphyrin (ZnPP). Conclusion CR effectively ameliorated insulin resistance, hyperglycemia, and dyslipidemia, and its mechanism of action may be at least partially, mediated through HO-1 activation via erythrocyte metabolic regulation. This study provided further evidences for the historical use of CR in the therapy of metabolic diseases. These results highlighted the potential of CR as a novel HO-1 agonist for the development of innovative treatments for GLD.
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CRYSTENGCOMM
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2020
·Vol. 22
·期 19
·3361-3370
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IF 3.117
Yini Mao,Li Jiang,Pengfei Xian,Qiongfen Fu,Shanshan Hu,Jun Yang
A graphical abstract is available for this content
研究领域:
材料科学
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光学
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NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
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2023
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IF 3.6
Zhang Yuying,Zhang Pingping,Zhang Xin,Liu Ye
Honokiol, a bioactive component found in Magnolia officinalis , has shown in protecting against ischemic stroke in animal models. However, its poor water solubility has limited its clinical applications. In this study, we introduced a hydrophilic building block on the aromatic ring of honokiol, resulting in the synthesis of four new compounds (HH-A, -B, -C and -D) with significantly improved water solubility. We then investigated the neuroprotective effects of these compounds in mouse and rat models of transient middle cerebral artery occlusion/reperfusion (tMCAO/R) brain injury. Among the compounds tested, HH-A, also known as (S)-6-((3′,5-diallyl-2,4′-dihydroxy-[1,1′-biphenyl]-3-yl)amino)-6-oxohexane-1,5-diaminium chloride, showed the most promising results. HH-A was found to significantly reduced the infarct volume and brain edema in mice. It also outperformed the other three compounds and honokiol, even surpassing the effects of edaravone dexborneol. Additionally, HH-A demonstrated dose-dependent improvements in body weight, neurological deficits, and infarct volume. Further analysis in tMCAO/R rat model revealed that HH-A treatment led to significant upregulations of Nrf2 and HO-1 in the brain. HH-A also significantly reduced the expression of HNE, and exhibited anti-apoptotic effects by decreasing the expression of Bax and increasing the expression of Bcl-2. This was further supported by a decrease in the number of TUNEL positive cells. Taken together, the neuroprotective effects of HH-A may be attributed to its ability to target the Nrf2/HO-1 signaling pathway, leading to reduced oxidative stress and apoptosis in the brain. These findings suggest that HH-A has potential as a therapeutic agent for the treatment of ischemic stroke.
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RENAL FAILURE
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2023
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IF 3
Chenlei Lv,Tianyang Cheng,Bingbing Zhang,Ke Sun,Keda Lu
Objectives: Diabetic nephropathy (DN) is the most common microvascular complication of diabetes mellitus. This study investigated the mechanism of triptolide (TP) in podocyte injury in DN.Methods: DN mouse models were established by feeding with a high-fat diet and injecting with streptozocin and MPC5 podocyte injury models were induced by high-glucose (HG), followed by TP treatment. Fasting blood glucose and renal function indicators, such as 24 h urine albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and kidney/body weight ratio of mice were examined. H&E and TUNEL staining were performed for evaluating pathological changes and apoptosis in renal tissue. The podocyte markers, reactive oxygen species (ROS), oxidative stress (OS), serum inflammatory cytokines, nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway-related proteins, and pyroptosis were detected by Western blotting and corresponding kits. MPC5 cell viability and pyroptosis were evaluated by MTT and Hoechst 33342/PI double-fluorescence staining. Nrf2 inhibitor ML385 was used to verify the regulation of TP on Nrf2.Results: TP improved renal function and histopathological injury of DN mice, alleviated podocytes injury, reduced OS and ROS by activating the Nrf2/heme oxygenase-1 (HO-1) pathway, and weakened pyroptosis by inhibiting the nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome pathway. In vitro experiments further verified the inhibition of TP on OS and pyroptosis by mediating the Nrf2/HO-1 and NLRP3 inflammasome pathways. Inhibition of Nrf2 reversed the protective effect of TP on MPC5 cells.Conclusions: Overall, TP alleviated podocyte injury in DN by inhibiting OS and pyroptosis via Nrf2/ROS/NLRP3 axis.
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Neural Regeneration Research
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2023
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IF 6.1
Jingwen Jiang,Hong Pan,Fanxia Shen,Yuyan Tan,Shengdi Chen
Alzheimer’s disease is a progressive neurological disorder characterized by cognitive decline and chronic inflammation within the brain. The ketogenic diet, a widely recognized therapeutic intervention for refractory epilepsy, has recently been proposed as a potential treatment for a variety of neurological diseases, including Alzheimer’s disease. However, the efficacy of ketogenic diet in treating Alzheimer’s disease and the underlying mechanism remains unclear. The current investigation aimed to explore the effect of ketogenic diet on cognitive function and the underlying biological mechanisms in a mouse model of Alzheimer’s disease. Male amyloid precursor protein/presenilin 1 (APP/PS1) mice were randomly assigned to either a ketogenic diet or control diet group, and received their respective diets for a duration of 3 months. The findings show that ketogenic diet administration enhanced cognitive function, attenuated amyloid plaque formation and proinflammatory cytokine levels in APP/PS1 mice, and augmented the nuclear factor-erythroid 2-p45 derived factor 2/heme oxygenase-1 signaling pathway while suppressing the nuclear factor-kappa B pathway. Collectively, these data suggest that ketogenic diet may have a therapeutic potential in treating Alzheimer’s disease by ameliorating the neurotoxicity associated with Aβ-induced inflammation. This study highlights the urgent need for further research into the use of ketogenic diet as a potential therapy for Alzheimer’s disease.
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Frontiers in Bioengineering and Biotechnology
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2023
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IF 5.7
Xiong Liping,Bao Han,Li Size,Gu Deao,Li Yuyang,Yin Qianwen,Li Wen,Miao Leiying,Liu Chao
Oxidative stress is closely linked to the etiology of temporomandibular joint osteoarthritis. (TMJ-OA) and is an important therapeutic target. Cerium oxide nanoparticles (CNPs) have been broadly studied owing to their powerful antioxidant properties and potential preventive and therapeutic effects against chronic diseases. The current study was designed to explore the protective effects of CNPs on the progression of TMJ-OA and their potential mechanisms. We detected the ability of CNPs to eliminate reactive oxygen species (ROS) in chondrocytes. Moreover, their protective effects on chondrocytes were detected in the level of gene and protein. Furthermore, TUNEL assay, histology and safranin O-fast green staining were used to detect the beneficial effects of CNPs on cartilage explants. The mechanism of CNPs, protecting condylar cartilage by reducing inflammation, was further explored by knocking down the Nuclear factor-erythroid 2-related factor (Nrf2) gene. CNPs could reduce the ROS levels in chondrocytes and cartilage explants and reverse the IL-1β-induced imbalance of cartilage matrix metabolism and apoptosis. The protective effects of CNPs on cartilage were lost after key antioxidant factors including Nrf2 and heme-oxygenase 1(HO-1) were significantly reduced. In conclusion, this study demonstrated for the first time that activating the Nrf2/HO-1 signaling pathway by CNPs might have therapeutic potential for TMJ-OA.
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CHEMICAL ENGINEERING JOURNAL
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2022
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IF 16.744
Quanfa Zhong,Zhong Zhang,Qinglong Fu,Jin Yu,Xiaoting Liao,Jianshu Zhao,Di He
Cl 2 •− can be the dominant radical species when high salinity wastewater is treated by advanced oxidation processes (AOPs). In this study, the steady-state concentrations of HO • , Cl • and Cl 2 •− were determined during the Fenton treatment of two landfill leachate concentrates with significantly different Cl − concentrations (XPNF: 1406 mg/L; SNNF: 8036 mg/L). Based on the steady-state concentrations of the radical species and measured second-order rate constants with dissolved organic matters (DOM), HO • accounted for 76.2% of DOM transformation in XPNF, while Cl 2 •− accounted for 96.5% in SNNF. The DOM transformation dominated by HO • or Cl 2 •− was then thoroughly compared to investigate the reactivities of HO • and Cl 2 •− with DOM at molecular level using high-resolution mass spectrometry. The results showed that formulas with low oxidation degree (O/C < 0.5) were preferentially removed by HO • and HO • was more reactive towards compounds with high saturation degree (H/C > 1.5) compared with Cl 2 •− . In contrast, Cl 2 •− was more reactive to the compounds with lower saturation level (H/C < 1.5) and the reaction of Cl 2 •− with DOM was less dependent on DOM oxidation degree. In addition, HO • preferentially reacted with the CHON compounds with low N content, while Cl 2 •− was more reactive to CHON compounds with higher N content compared with HO • . To our knowledge, this is the first study to distinguish the difference in the reactivity of HO • and Cl 2 •− towards DOM at molecular level.
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CHEMISTRY & BIODIVERSITY
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2021
·Vol. 18
·期 4
·e2001007
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IF 2.408
Yan Zhao,Yu Wang,Min Zhang,Yugang Gao,Zhaowei Yan
Ginsenosides (20 S )-Rg3 and (20 R )-Rg3 are famous rare ginsenosides from red ginseng, and their configurations in C-20 are different. This study aimed to investigate the protective mechanism of ginsenosides (20 S )-Rg3 and (20 R )-Rg3 on H 2 O 2 -induced H9C2 cells and compare their activity. The results showed that the ginsenosides (20 S )-Rg3 and (20 R )-Rg3 could increase the cell activity and the levels of GSH-Px, SOD and CAT, and decrease activities of LDH, MDA and ROS. Further studies showed that ginsenosides (20 S )-Rg3 and (20 R )-Rg3 could prevent oxidative stress injury of H9C2 cells by H 2 O 2 through the Keap-1/Nrf2/HO-1 pathway. But the ML385 counteracts these effects. Interestingly, among these results, ginsenoside (20 R )-Rg3 was superior to (20 S )-Rg3, indicating that ginsenoside (20 R )-Rg3 have a stronger effect of antioxidative stress. This study reflected that ginsenoside (20 R )-Rg3 could be used as a potential Nrf2 activator and a safe effective Chinese herbal monomer in the treatment of cardiovascular disease.
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Frontiers in Pharmacology
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2020
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IF 4.225
Yao He,Sun Jingyu,Wei Jie,Zhang Xin,Chen Bing,Lin Yajun
Over recent years, an increasing number of studies have confirmed that the occurrence and development of vascular pathological changes are closely related to oxidative stress and the inflammatory response of the vascular endothelium. Kaempferol is the most common flavonoid compound found in fruits and vegetables. Our present research identified that kaempferol had the capability to protect the vascular endothelium in a mouse model of vascular injury and explored the specific mechanisms underlying these effects by investigating oxidative stress, the extent of cardiovascular injury, and inflammatory markers such as NF-κB, TNF-α, IL-6, and the Nrf2/HO-1 signaling pathway. Analysis showed that kaempferol reduced oxidative stress and inflammation mediated by H2O2 and paraquat, respectively, both in vitro and in vivo. Furthermore, kaempferol suppressed the levels of TNF-α and IL-6, and the activation of NF-κB, in aortic tissues and human umbilical vein endothelial cells (HUVECs). Finally, we observed that kaempferol corrected the levels of antioxidants and elevated the protein levels of Nrf2 and HO-1 in aortic tissues and HUVECs. Collectively, our findings prove that kaempferol protects blood vessels from damage induced by oxidative stress and inflammation and that the Nrf2/HO-1 signaling pathway plays a key role in mediating these effects.
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Advanced Healthcare Materials
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2024
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IF 10
Yu Yang,Jiang Du,Jingjing Gan,Xiang Song,Jiaxin Shu,Chaoli An,Li Lu,Hui Wei,Junyi Che,Xiaozhi Zhao
Reactive oxygen species (ROS) scavenging of nanozymes toward acute kidney injury (AKI) is a current promising strategy, however, the glomerular filtration barrier (GFB) limits their application for treating kidney related diseases. Here, a neutrophil-mediated delivery system able to hijack neutrophil to transport nanozyme-loaded cRGD-liposomes to inflamed kidney for AKI treatment by cRGD targeting integrin αvβ1 is reported. The neutrophil-mediated nanozyme delivery system demonstrated great antioxidant and anti-apoptosis ability in HK-2 and NRK-52E cell lines. Moreover, in ischemia-reperfusion (I/R) induced AKI mice, a single dose of LM@cRGD-LPs 12 h post-ischemia significantly reduces renal function indicators, alleviates renal pathological changes, and inhibits apoptosis of renal tubular cells and the expression of renal tubular injured marker, thus remarkably reducing the damage of AKI. Mechanistically, the treatment of LM@cRGD-LPs markedly inhibits the process of Nrf2 to the nucleus and reduces the expression of the downstream HO-1, achieves a 99.51% increase in renal tissue Nrf2 levels, and an 86.31% decrease in HO-1 levels after LM@cRGD-LPs treatment. In short, the strategy of neutrophil-mediated nanozyme delivery system hold great promise as a potential therapy for AKI or other inflammatory diseases.
研究领域:
肾病学
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药学
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生物技术
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分子生物学
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治疗学
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Food Bioscience
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2024
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IF 4.8
Yueyao Gui,Bing Zheng,Hairong Huang,Jianhua Xie,Yi Chen,Jialuo Shan,Xingxing Chang,Xiaobo Hu,Qiang Yu
Alcoholic liver disease (ALD) is characterized by inflammation and oxidative stress induced by excessive alcohol consumption. It is necessary to find a way to use natural active substances to alleviate the liver damage caused by alcohol. The object of this study was to investigate the beneficial effects of pure Polygomatum cyrtonema polysaccharide (PCP-80%) on ALD, and to explore its possible mechanism from the aspect of oxidative stress, inflammation and intestinal microbiota. The results demonstrated that PCP-80% effectively reduced serum biochemical index level and improved liver disease induced by acute alcohol exposure. Furthermore, PCP-80% showed promising outcomes in mitigating oxidative stress and liver inflammation associated with ALD. This might relate to the inhibition of NF-κB pathway and the activation of Keap1/HO-1 pathway. Additionally,PCP-80% enhanced the intestinal barrier and elevated the levels of propionic acid in the colon contents. It also partially reversed the alcohol-induced disturbances in the intestinal microbiome. Overall, PCP-80% exhibited significant therapeutic potential in alleviating acute alcoholic liver injury by reducing oxidative stress, inflammation, and relieving disturbances in the intestinal microbiome. These findings presented a novel approach for the treatment of acute alcoholic liver injury, offering prospects for improving disease prognosis.
研究领域:
药理学
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肝病学
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胃肠病学
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免疫学
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微生物学
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