JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2015
·
IF 2.912
Chuanyang Su,Xiaomin Xia,Qiong Shi,Xiufang Song,Juanli Fu,Congxue Xiao,Hongjun Chen,Bin Lu,Zhiyin Sun,Shanmei Wu,Siyu Yang,Xuegang Li,Xiaoli Ye,Erqun Song,Yang Song
Neohesperidin dihydrochalcone (NHDC), a sweetener derived from citrus, belongs to the family of bycyclic flavonoids dihydrochalcones. NHDC has been reported to act against CCl4-induced hepatic injury, but its mechanism is still unclear. We first discovered that NHDC showed a strong ability to scavenge free radicals. In addition, NHDC induces the phase II antioxidant enzymes heme oxygenase 1 (HO-1) and NAD(P)H/quinone oxidoreductase 1 (NQO1) through the activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/antioxidant response element (ARE) signaling. Further assays demonstrated that NHDC induces accumulation of Nrf2 in the nucleus and augmented Nrf2-ARE binding activity. Moreover, NHDC inhibits the ubiquitination of Nrf2 and suggests the modification of Kelch-like ECH-associated protein 1 (Keap1) and the disruption of the Keap1/Nrf2 complex. c-Jun N-terminal kinase (JNK) and p38 but not extracellular signal-regulated protein kinase (ERK) phosphorylations were up-regulated by NHDC treatment. Taken together, NHDC showed its protective antioxidant effect against CCl4-induced oxidative damage via the direct free radical scavenging and indirect Nrf2/ARE signaling pathway.
研究领域:
药理学
·
毒理学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Environmental Chemical Engineering
·
2023
·
IF 7.7
Yuan Chen,Yuancai Chen,Yexia Qin
In the present study, we found that nanoparticles (Pd-NPs) were biosynthesized by Bacillus wiedmannii MSM ( B. wiedmannii MSM) with endogenous carbon under O 2 condition, and more favorablity under N 2 purging condition. XRD results indicated that crystal planes of Pd-NPs were attributed to Pd 0 (111), Pd 0 (200), Pd 0 (220), and Pd 0 (311), respectively. TEM and STEM-EDX results showed that the bio-reduction of Pd (II) ( k pd,1 =4.799 min −1 ) occurred predominately in periplasm space. FTIR results showed that the -COOH, -OH, and -NH 2 were the main groups participating in the removal of Pd (II). The aerobic reduction of Pd (II) by B. wiedmannii MSM was proposed, including extracellular superoxide radicals produced by NAD(P)H oxidases , endogenous electron donors, and O 2 -insensitive hydrogenase. These studies provide new methods and insights for reduction of Pd (II).
研究领域:
环境科学
·
材料科学
·
微生物学
·
化学
✓ 已验证
产品关联
DOI
高影响因子
Environmental Science-Nano
·
2023
·
IF 7.3
Shuoli Ma,Wen-Xiong Wang
Nano-Zn (nZnO) has been increasingly applied in different fields, but the mechanisms of their uses as nutritional sources are less understood. Our study presents a regulatory mechanism of intestinal microbiota and structure mediated by nano-Zn, which subsequently improves the health and growth of fish. Fish diets were supplemented with 60 mg Zn kg−1 ZnSO4 (metal salt as the control group), 60 mg Zn kg−1 nZnO (powder), or 170 mg Zn kg−1 nZnO (powder) and then fed to golden pompanos for 5 weeks. We employed a new analytical amplicon sequence variant (ASV) method to identify the bacterial species and achieved the first in situ spatial quantification of fish tissue samples. Our results indicated that 60 mg Zn kg−1 of dietary nZnO promoted the probiotic colonization (Lactic-acid bacilli spp.) in the intestine. Upon exposure to a higher nZnO dose (170 mg Zn kg−1), Brevinema and Mycoplasma colonized in the fish intestine as pro-inflammatory microorganisms, which activated the C5 isoprenoid biosynthesis pathway and NAD biosynthesis. Furthermore, dietary nZnO (60 mg Zn kg−1) up-regulated the expression of genes related to intestinal mucus secretion and accelerated the goblet cell renewal in the intestinal villi. At a dose of 170 mg Zn kg−1 nZnO, the fish intestine significantly down-regulated occludin and mucin gene expression while displaying lower villus height, villus area, and goblet cell numbers, which ultimately led to abnormal digestion and absorption and immune functions. The Mantel test confirmed that the intestinal microbial abundance was significantly correlated with the changes in the intestinal structure, and the value of villi-to-crypt ratio decreased with the increase in Vibrio abundance, which was validated by the key genes and serum biochemical indexes. Finally, nZnO could regulate the glucose and lipid metabolism of fish by regulating microorganisms. Our results provided important insights into the interaction between nZnO and fish intestinal microbial community and host.
研究领域:
水产养殖
·
微生物学
·
营养学
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分子生物学
✓ 已验证
产品关联
DOI
高影响因子
JOURNAL OF COLLOID AND INTERFACE SCIENCE
·
2024
·
IF 9.4
Xueping Yan,Peng Jing,Zitian Zhuang,Jianing Zhang,Haiming Chen,Tifeng Xia,Ke Jiang
As an alternative to chemotherapy, emerging gas therapy is considered a “green” treatment due to its minimal side effects. However, even typical gas molecules like nitric oxide (NO) face challenges such as a very short half-life (1.5–6 min), poor targeting, and limited therapeutic effects. This study employs a one-pot method to simultaneously encapsulate the NO donor L-arginine (L-Arg) and the H 2 O 2 precursor Vitamin K3 (VK3) into the pores of zeolitic imidazolate framework-8 (ZIF-8), achieving their co-delivery to tumor sites to address these issues. Furthermore, ZIF-8 is functionalized with hyaluronic acid (HA) to impart active targeting properties to tumor tissues. In the acidic tumor microenvironment, pH-sensitive ZIF-8 degrades, releasing VK3 and L-Arg. Under the action of the NAD(P)H quinone oxidoreductase-1 (NQO1) enzyme, VK3 generates H 2 O 2 , increasing oxidative stress levels in the tumor microenvironment, and reacts with L-Arg to produce NO, thereby achieving tumor oxidative stress-based gas therapy. Both in vitro and in vivo experiments showed good tumor treatment effects, with a tumor inhibition rate of up to 90.5 % and minimal impact on normal tissues and organs. This approach demonstrates efficient loading, controlled release, and significant anti-tumor performance, offering new insights into gas and reactive oxygen species (ROS) synergistic therapy.
研究领域:
癌症治疗
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药物递送系统
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材料科学
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生物医学工程
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药学化学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Scientific Reports
·
2017
·Vol. 7
·期 1
·1-11
·
IF 4.259
Zhao Hongting,Li Huihui,Hao Shuangying,Chen Jiping,Wu Jing,Song Chuanhui,Zhang Meng,Qiao Tong,Li Kuanyu
Friedreich ataxia is a progressive neurodegenerative disease caused by the expansion of GAA trinucleotide repeats within the first intron of the FXN gene, which encodes frataxin. The pathophysiology of the disease is thought to be derived from the decrease of Fe-S cluster biogenesis due to frataxin deficiency. There is currently no effective treatment for the disease. In our study, we demonstrated that treatment with the mitochondrion-targeted peptide SS-31 reduced frataxin deficiency-induced oxidative stress in lymphoblasts and fibroblasts derived from patients. Interestingly, SS-31 treatment translationally upregulated the protein level of frataxin in a dose-dependent manner. Furthermore, SS-31 treatment increased the enzymatic activities of the iron-sulphur enzymes, including aconitase and complex II and III of the respiratory chain. Further evaluation of the quality of mitochondria showed that mitochondrial membrane potential, ATP content, NAD + /NADH, and the morphology of mitochondria all improved. Our results suggest that SS-31 might potentially be a new drug for the early treatment of Friedreich ataxia.
研究领域:
神经退行性疾病
·
分子生物学
·
线粒体生物学
·
遗传病
✓ 已验证
DOI
PubMed
高影响因子
Advanced Science
·
2023
·Vol. 10
·期 14
·2207448
·
IF 15.1
Jiahui Yan,Jingwen Zhang,Yanan Wang,Hong Liu,Xueping Sun,Aixin Li,Pengfei Cui,Liangmin Yu,Xuefeng Yan,Zhiyu He
Pyroptosis, systemic inflammation, and mitochondrial apoptosis are the three primary contributors to sepsis's multiple organ failure, the ultimate cause of high clinical mortality. Currently, the drugs under development only target a single pathogenesis, which is obviously insufficient. In this study, an acid-responsive hollow mesoporous polydopamine (HMPDA) nanocarrier that is highly capable of carrying both the hydrophilic drug NAD + and the hydrophobic drug BAPTA-AM, with its outer layer being sealed by the inflammatory targeting peptide PEG-LSA, is developed. Once targeted to the region of inflammation, HMPDA begins depolymerization, releasing the drugs NAD + and BAPTA-AM. Depletion of polydopamine on excessive reactive oxygen species production, promotion of ATP production and anti-inflammation by NAD + replenishment, and chelation of BAPTA (generated by BA-AM hydrolysis) on overloaded Ca 2+ can comprehensively block the three stages of sepsis, i.e., precisely inhibit the activation of pyroptosis pathway (NF- κ B-NLRP3-ASC-Casp-1), inflammation pathway (IL-1 β , IL-6, and TNF- α ), and mitochondrial apoptosis pathway (Bcl-2/Bax-Cyt-C-Casp-9-Casp-3), thereby restoring intracellular homeostasis, saving the cells in a state of “critical survival,” further reducing LPS-induced systemic inflammation, finally restoring the organ functions. In conclusion, the synthesis of this agent provides a simple and effective synergistic drug delivery nanosystem, which demonstrates significant therapeutic potential in a model of LPS-induced sepsis.
研究领域:
药理学
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纳米技术
·
免疫学
·
细胞生物学
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治疗学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Small
·
2024
·
IF 13
Lihua Chen,Hui Ming,Bowen Li,Chen Yang,Shanshan Liu,Yajie Gao,Tingting Zhang,Canhua Huang,Tingyuan Lang,Zhuo Yang
Cancer metastasis poses significant challenges in current clinical therapy. Osthole (OST) has demonstrated efficacy in treating cervical cancer and inhibiting metastasis. Despite these positive results, its limited solubility, poor oral absorption, low bioavailability, and photosensitivity hinder its clinical application. To address this limitation, a glutathione (GSH)-responded nano-herb delivery system (HA/MOS@OST&L-Arg nanoparticles, HMOA NPs) is devised for the targeted delivery of OST with cascade-activatable nitric oxide (NO) release. The HMOA NPs system is engineered utilizing enhanced permeability and retention (EPR) effects and active targeting mediated by hyaluronic acid (HA) binding to glycoprotein CD44. The cargoes, including OST and L-Arginine (L-Arg), are released rapidly due to the degradation of GSH-responsive mesoporous organic silica (MOS). Then abundant reactive oxygen species (ROS) are produced from OST in the presence of high concentrations of NAD(P)H quinone oxidoreductase 1 (NQO1), resulting in the generation of NO and subsequently highly toxic peroxynitrite (ONOO − ) by catalyzing guanidine groups of L-Arg. These ROS, NO, and ONOO − molecules have a direct impact on mitochondrial function by reducing mitochondrial membrane potential and inhibiting adenosine triphosphate (ATP) production, thereby promoting increased apoptosis and inhibiting metastasis. Overall, the results indicated that HMOA NPs has great potential as a promising alternative for the clinical treatment of cervical cancer.
研究领域:
药学
·
纳米技术
·
癌症研究
·
药物递送系统
·
生物化学
✓ 已验证
DOI
PubMed
高影响因子
ADVANCED FUNCTIONAL MATERIALS
·
2025
·
IF 19
Shiyao Guo,Mingyue Zhang,Ke Zhang,Xiaotong Lu,Peiran Chen,Bangliu Yang,Xueqian Wang,Yuhong Zhuo,Dongqin Yu,Chao Qi,Kaiyong Cai
Osteoporosis compromises bone repair by generating a dysregulated microenvironment marked by excessive accumulation of reactive oxygen species (ROS) and a reduced pH. This pathological state leads to mitochondrial dysfunction, impaired osteogenic differentiation, and excessive activation of osteoclasts. In this study, a ROS-responsive titanium implant coating composed of calcium carbonate-mineralized nicotinamide mononucleotide (NMN) nanoparticles, lipoic acid-modified gelatin (LAMG), and sodium alginate (SA) is developed, designed to enhance osseointegration through dual synergistic mechanisms. First, the LAMG hydrogel effectively scavenges excess ROS, while calcium carbonate neutralizes H + ions and restores physiological pH levels, thereby reducing acid-induced bone resorption and inhibiting osteoclast activity. Second, ROS and H + ions-triggered release of NMN enhances the intracellular NAD⁺/NADH ratio in bone marrow mesenchymal stem cells, activates the SIRT1 signaling pathway, restores mitochondrial function, and promotes osteogenic differentiation. By concurrently remodeling the pathological bone microenvironment and repairing mitochondrial dysfunction, this multifunctional coating suppresses osteoclast-mediated bone resorption while facilitating osteoblast formation, thereby enhancing peri-implant osseointegration under osteoporotic conditions. This strategy not only presents a promising therapeutic approach for functionalizing titanium implants but also offers a potentially translatable platform for treating osteoporotic bone defects.
研究领域:
生物材料
·
组织工程
·
骨科
·
再生医学
·
纳米医学
·
骨骼生物学
·
生物医学工程
✓ 已验证
产品关联
DOI
高影响因子
CELLULAR SIGNALLING
·
2021
·
IF 4.315
Hao Huang,Xielan Kuang,Xiaobo Zhu,Hao Cheng,Yuxiu Zou,Han Du,Han Tang,Linbin Zhou,Jingshu Zeng,Huijun Liu,Jianhua Yan,Chongde Long,Huangxuan Shen
Retinal ischemia-reperfusion (I/R) often results in intractable visual impairments, where blood retinal barrier (BRB) homeostasis mediated by retinal pigment epithelium (RPE) and retinal microvascular endothelium (RME) is crucial. However, strategies targeting the BRB are limited. Thus, we investigated the inconclusive effect of lycopene (LYC) in retinal protection under I/R. LYC elevated cellular viability and reversed oxidative stress in aRPE-19 cells/hRME cells under I/R conditions based on oxygen-glucose deprivation (OGD) in vitro . Molecular analysis showed that LYC promoted NRF2 expression and enhanced the downstream factors of the KEAP1/NRF2/ARE pathway: LYC increased the activities of antioxidants, including SOD and CAT , whereas it enhanced the mRNA expression of HO-1 ( ho-1 ) and NQO-1 ( nqo-1 ). The activation resulted in restrained ROS and MDA. On the other hand, LYC ameliorated the damage to retinal function and morphology in a mouse I/R model, which was established by unilateral ligation of the left pterygopalatine artery/external carotid artery and reperfusion . LYC promoted the expression of NRF2 in both the neural retina and the RPE choroid in vivo . This evidence revealed the potential of LYC in retinal protection under I/R, uncovering the pharmacological effect of the KEAP1/NRF2/ARE pathway in BRB targeting. The study generates new insights into scientific practices in retinal research.
研究领域:
眼科学
·
药理学
·
分子生物学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF HAZARDOUS MATERIALS
·
2022
·
IF 14.224
Zhiyan Yan,Chenrui Liu,Yun Liu,Xiaoqian Tan,Xinyue Li,Yan Shi,Chunlian Ding
Cr(VI) contaminated water usually contains other contaminants like engineered nanomaterials (ENMs). During the process of microbial treatment , the inevitable interaction of Cr(VI), ENMs, and microorganisms probably determines the efficiency of Cr(VI) biotransformation , however, the corresponding information remains elusive. This study investigated the interaction of ZnO nanoparticles (NPs), Cr(VI), and Pannonibacter phragmitetu s BB (hereafter BB), which changed the process of microbial Cr(VI) reduction. ZnO NPs inhibited Cr(VI) reduction, but had no effect on bacterial viability. In particular, Cr(VI) induced BB to produce organic acids and to drive Zn 2+ dissolution from ZnO NPs inside and outside of cells. The dissolved Zn 2+ not only promoted Cr(VI) reduction to Cr(V)/Cr(IV) by strengthening sugar metabolism and inducing increase in NAD(P)H production, but also hindered Cr(V)/Cr(IV) transformation to Cr(III) through down-regulating Cr(VI) reductase genes. A novel bacterial driven ROS scavenging mechanism leading to the inhibition of Cr(VI) reduction was elucidated. Specifically, the accumulated Cr(VI) and Cr(V)/Cr(IV) formed a redox dynamic equilibrium, which triggered the disproportionation of superoxide radicals mimicking superoxide dismutase through the flip-flop of Cr(VI) and Cr(V)/Cr(IV) in bacterial cells. This study provided a realistic insight into design the applicability of biological remediation technology for Cr(VI) contaminant and evaluating environmental risks of ENMs.
研究领域:
环境科学
·
微生物学
·
纳米技术
·
生物修复
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Drug Design Development and Therapy
·
2022
·
IF 4.319
Wen-Gang Chen,Sa-Sa Zhang,Shu Pan,Zhong-Fang Wang,Jin-Ying Xu,Xue-He Sheng,Qin Yin,Yi-Jin Wu
Background Studies have found that α-mangostin (MG) can relieve experimental arthritis by activating cholinergic anti-inflammatory pathway (CAP). It affects the polarization of macrophages and the balance of related immune cell subpopulations, but the specific mechanism is still unclear. It has been found that silent information regulator 1 (SIRT1) is closely related to macrophage activity. The purpose of this study is to explore the mechanism of MG intervening in macrophage polarization during treatment of early adjuvant-induced (AIA) rats through the CAP-SIRT1 pathway.Methods We investigated the polarization of M1 macrophages and the differentiation of Th1 in AIA rats by flow cytometry. Activity of acetylcholinesterase (AChE) and the level of nicotinic adenine dinucleotide (NAD+) in serum were also detected, and immunohistochemical was used to detect the levels of α7 nicotinic cholinergic receptor (α7nAChR) and SIRT1. Then in macrophages, the molecular mechanism of MG regulating the abnormal activation of macrophages in rats with early AIA through the CAP-SIRT1 pathway was studied.Results MG can significantly inhibit the polarization of M1 macrophages and the differentiation of Th1 in AIA rats in the acute phase of inflammation. MG can significantly inhibit the activity of AChE and increase the level of NAD+, thereby further up-regulated the expression levels of α7nAChR and SIRT1. Meanwhile, MG inhibited nuclear factor-κB (NF-κB)-mediated inflammation by activating the CAP-SIRT1 pathway in macrophages.Conclusion In summary, the stimulation of MG induced CAP activation, which up-regulated SIRT1 signal, and thereby inhibited M1 polarization through the NF-κB pathway, and improved the pathological immune environment of early-stage AIA rats.
研究领域:
免疫学
·
药理学
·
风湿病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF COLLOID AND INTERFACE SCIENCE
·
2024
·
IF 9.4
Fang Liu,Yaru Li,Yao Li,Zheng Wang,Xin Li,Yancheng Liu,Yanjun Zhao
The clinical translation of the anticancer drug β -lapachone (LAP) has been limited by the narrow therapeutic window. Stimuli-responsive anticancer drug delivery systems have gained tremendous attention in recent years to alleviate adverse effects and enhance therapeutic efficacy. Here, we report a dual pH- and enzyme-responsive nanocarrier to address the above issue of LAP. In detail, the epigallocatechin gallate (EGCG) and ferric ions were employed to engineer nanoscale ferric ion-polyphenol complexes where LAP was physically encapsulated therein. The coordination bond between Fe 3+ and the catechol moiety of EGCG was sensitive to the low pH, enabling the triggered cargo release in the acidic endosomes/lysosomes. Afterward, the released LAP was activated by the overexpressed NAD(P)H: quinone oxidoreductase 1 (NQO1) and ferroptosis suppressor protein 1 (FSP1) in the tumor cells, followed by the generation of reactive oxygen species (ROS), and the induction of oxidative stress and apoptotic cell death. Meanwhile, EGCG could upregulate gasdermin E (GSDME), and ferric ions were involved in the Fenton reaction. Hence, EGCG and ferric ions could sensitize the toxicity of LAP through the induction of multiple cell death pathways ( e.g ., pyroptosis, ferroptosis, apoptosis, and necroptosis). The current work enlarged the LAP’s therapeutic window via controlled cargo release and vehicle sensitization.
研究领域:
药学
·
纳米技术
·
癌症治疗
·
药物递送系统
·
细胞死亡机制
✓ 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）