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Food Bioscience · 2023 · IF 5.2

The structural characterization of polysaccharides from three cultivars of Moringa oleifera Lam. root and their effects on human intestinal microflora

Linlin Jia,Xiaoqiang Peng,Zeyuan Deng,Bing Zhang,Hongyan Li

Moringa oleifera Lam. is an edible plant . In this experiment, three kinds of small molecular weight Polysaccharides (MRP-D, MRP-P, MRP-H) were extracted from Dai-Jia ecology, Pkm-3 and Hong-he 1 Moringa oleifera root that were cultivated in three regions of Yunnan Province. The Moringa oleifera root Polysaccharides (MRPs) were identified to contain β-(1 → 3)-Glucose structure, without triple-helical conformation. In vitro fermentation experiment showed the MRPs increased the content of short-chain fatty acids (3–5-fold) and the abundance of beneficial microflora such as Bacteroidetes and decreased the abundance of harmful microflora such as Proteobacteria at the same time. The composition and effects on the human intestinal microflora of MRPs were different, indicating that the planting regions would affect the composition and function of the bioactives. These results provide an experimental basis for the industrial layout of Moringa oleifera and the application of MRPs in food processing.

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FOOD RESEARCH INTERNATIONAL · 2022 · IF 7.425

Microwave bag cooking affects the quality, glucosinolates content and hydrolysate production of broccoli florets

Wenxiu Zheng,Wenhao Wang,Desheng Fu,Tianyu Zhang,Zhengrui Liang,Ling Yan,Changhong Liu,Lei Zheng

Appropriate processing and cooking technologies can effectively improve the content of bioactive compounds in vegetables. The effects of microwave bag cooking on broccoli floret quality attributes, glucosinolates (GLSs) content and hydrolysate production were investigated in this study. Microwave bag cooking not only preserved the color of the florets, but also enhanced the total phenolic and flavonoid content, as well as total chlorophyll and ascorbic acid content. Furthermore, the majority of the microorganisms were inactivated, and the structure of the florets was greatly destroyed, thereby increasing antioxidant capacity and promoting the release of GLSs and myrosinase activity in the florets. Moreover, microwave bag cooking significantly enriched the sulforaphane (SFN) and indole-3-carbinol (I3C) production of broccoli florets in the meantime, demonstrating that it was a convenient and quick cooking option to satisfy the requirements of modern consumers.

CAS / MDL: 700-06-1 4478-93-7
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Materials Today Bio · 2022 · IF 10.761

Redox homeostasis modulation using theranostic AIE nanoparticles results in positive-feedback drug accumulation and enhanced drug penetration to combat drug-resistant cancer

Shaoqing Chen,Ziyu Wang,Li Liu,Yuting Li,Xinye Ni,Hong Yuan,Cheng Wang

Drug-resistant cancers usually have multiple barriers to compromise the effect of therapies, of which multidrug-resistance (MDR) phenotype as the intracellular barrier and dense tumor matrix as the extracellular barrier, significantly contribute to the poor anticancer performance of current drug delivery systems (DDS). Here in this study, we fabricated a novel aggregation-induced emission (AIE)-active polymer capable of self-assembling into ultrasmall nanoparticles (∼20 ​nm) with D-alpha Tocopheryl Polyethylene Glycol Succinate (TPGS), for dual-encapsulating of doxorubicin (Dox) and sulforaphane (SFN) (AT/Dox/SFN). It revealed that redox homeostasis modulation of MDR cells (MCF-7/Adr) using AT/Dox/SFN can trigger mitochondria damage and ATP deficiency, which reverse the MDR phenotype of MCF-7/Adr cells to afford enhanced cellular uptake of both drug and DDS in a positive-feedback manner. The enhanced cellular drug accumulation further initiates the “neighboring effect” for improved drug penetration. Using this strategy, the growth of in vivo MCF-7/Adr tumors can be effectively inhibited at a low dosage (1/5) of doxorubicin (Dox) as compared to free Dox. In summary, we offer a new approach to overcome both the intracellular and extracellular barriers of drug-resistant cancers and elucidate the potential action mechanisms, which are beneficial for better cancer management.

CAS / MDL: 4478-93-7
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ENVIRONMENT INTERNATIONAL · 2022 · IF 13.352

Zinc oxide/graphene oxide nanocomposites efficiently inhibited cadmium-induced hepatotoxicity via releasing Zn ions and up-regulating MRP1 expression

Yun Liu,Xue Wang,Bo Si,Tong Wang,Yun Wu,Ying Liu,Yemian Zhou,Haiyang Tong,Xinwei Zheng,An Xu

Environmental cadmium (Cd) pollution has been verified to associated with various hepatic diseases, as Cd has been classified as one of the TOP 20 Hazardous Substances and liver is the main target of Cd poisoning. However, to design efficient hepatic antidotes with excellent detoxification capacity and reveal their underlying mechanism(s) are still challenges in Cd detoxification. Herein, ZnO/GO nanocomposites with favorable biocompatibility was uncovered their advanced function against Cd-elicited liver damage at the in situ level in vivo by 9.4 T magnetic resonance imaging (MRI). To explore the cellular detoxification mechanism, ZnO/GO nanocomposites was found to effectively inhibit the cyto- and geno-toxicity of Cd with the maximum antagonistic efficiency to be approximately 90%. Mechanistically, ZnO/GO nanocomposites competitively inhibited the cellular Cd uptake through releasing Zn ions, and significantly promoted Cd excretion via targeting the efflux pump of multidrug resistance associated protein1 (MRP1), which was confirmed by mass spectra and immunohistochemical analysis in kidney, a main excretion organ of Cd. Our data provided a novel approach against Cd-elicited hepatotoxic responses by constructed ZnO/GO nanocomposites both in vitro and in vivo , which may have promising application in prevention and detoxification for Cd poisoning.

CAS / MDL: 4478-93-7
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JOURNAL OF NUTRITIONAL BIOCHEMISTRY · 2022 · IF 6.117

Isothiocyanates attenuate immune checkpoint blockage therapy in gastric cancer via induction of PD-L1 expression

Qi Zhang,Wanshuang Cao,Chenying Yang,Lixia Hong,Shanshan Geng,Hongyu Han,Caiyun Zhong

The PD-1/PD-L1 immune checkpoint blockade therapy has shown revolutionary efficacy in the treatment of multiple cancers including gastric cancer. Isothiocyanates play important roles in cancer cell suppression and immunomodulation . However, the effects of isothiocyanates on immune checkpoint inhibitors are poorly understood in gastric cancer. The influence of three major isothiocyanates (sulforaphane, phenylethyl isothiocyanate, and benzhydryl isothiocyanate) on gastric cancer cell growth and PD-L1 expression was investigated. Syngeneic mouse models were administered by isothiocyanates and anti-PD-L1 monoclonal antibody , and the anti-tumor effects were assessed. The expression of PD-L1, proportion of lymphocytes and serum cytokine levels were detected to explore the underlying mechanisms. We found that PD-L1 expression was significantly induced by isothiocyanates which was associated with TAp63α up-regulation. We further revealed that TAp63α promoted PD-L1 through transcriptional activation . Combination treatment of isothiocyanates and anti-PD-L1 therapy weakened the sensitivity of gastric cancer cells to anti-PD-L1 drug. Moreover, in vivo studies illustrated that the interference effects of isothiocyanates on anti-PD-L1 antibody were related to PD-L1 expression and decreased infiltrating T lymphocytes in tumor bearing mouse hosts. Our findings provide novel insights as isothiocyanates could interfere with the successful application of immunotherapy in gastric cancer.

CAS / MDL: 4478-93-7
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ENVIRONMENTAL TOXICOLOGY · 2023 · IF 4.5

Effect and molecular mechanism of Sulforaphane alleviates brain damage caused by acute carbon monoxide poisoning:Network pharmacology analysis, molecular docking, and experimental evidence

Ao-Chun Yue,Xu-Dong Zhou,Hui-Ping Song,Xu-Han Liu,Ming-Jun Bi,Wei Han,Qin Li

Sulforaphane (SFN) has attracted much attention due to its ability on antioxidant, anti-inflammatory, and anti-apoptotic properties, while its functional targets and underlying mechanism of action on brain injury caused by acute carbon monoxide poisoning (ACOP) have not been fully elucidated. Herein, we used a systematic network pharmacology approach to explore the mechanism of SFN in the treatment of brain damage after ACOP. In this study, the results of network pharmacology demonstrated that there were a total of 81 effective target genes of SFN and 36 drug–disease targets, which were strongly in connection with autophagy–animal signaling pathway, drug metabolism, and transcription disorders in cancer. Upon the further biological function and KEGG signaling pathway enrichment analysis, a large number of them were involved in neuronal death, reactive oxygen metabolic processes and immune functions. Moreover, based on the results of bioinformatics prediction associated with multiple potential targets and pathways, the AMP-activated protein kinase (AMPK) signaling pathway was selected to elucidate the molecular mechanism of SFN in the treatment of brain injury caused by ACOP. The following molecular docking analysis also confirmed that SFN can bind to AMPKα well through chemical bonds. In addition, an animal model of ACOP was established by exposure to carbon monoxide in a hyperbaric oxygen chamber to verify the predicted results of network pharmacology. We found that the mitochondrial ultrastructure of neurons in rats with ACOP was seriously damaged, and apoptotic cells increased significantly. The histopathological changes were obviously alleviated, apoptosis of cortical neurons was inhibited, and the number of Nissl bodies was increased in the SFN group as compared with the ACOP group ( p < .05). Besides, the administration of SFN could increase the expressions of phosphorylated P-AMPK and MFN2 proteins and decrease the levels of DRP1, Caspase3, and Casapase9 proteins in the brain tissue of ACOP rats. These findings suggest that network pharmacology is a useful tool for traditional Chinese medicine (TCM) research, SFN can effectively inhibit apoptosis, protect cortical neurons from the toxicity of carbon monoxide through activating the AMPK pathway and may become a potential therapeutic strategy for brain injury after ACOP.

CAS / MDL: 4478-93-7
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FOOD CHEMISTRY · 2023 · IF 8.8

Facile preparation of biomimetic mineralized COFs based on magnetic silk fibroin and its effective extraction of sulforaphane from cruciferous vegetables

Guangyang Liu,Xuan Zhang,Jian Wang,Lingyun Li,Jiayong Cao,Chen Yin,Yuan Liu,Ge Chen,Jun Lv,Xiaomin Xu,Jing Wang,Xiaodong Huang,Donghui Xu

A novel biomimetic mineralized covalent organic framework (BM-COF) was prepared based on magnetic silk fibroin and a new sulforaphane pretreatment technology was constructed. First, metal coordination was performed on the surface of silk fibroin, and nanoparticles were deposited by in-situ mineralization after co-precipitation. Then, biomineralized COFs were prepared by in-situ self-assembly of a COF layer on Fe 3 O 4 @silk fibroin surface guided by interfacial directional growth technology. The BM-COFs had a multilayer structure, large specific surface area and pore volume, and superparamagnetic properties, which make them an ideal adsorbent. The adsorption of sulforaphane by BM-COFs is mainly multi-molecular layer adsorption and chemisorption, there might be electrostatic action, π-stacking and hydrogen bonding in the adsorption process. The composite material was successfully used for the pretreatment of sulforaphane in cruciferous vegetables. An extraction time of 30 min gave extraction efficiencies as high as 92%, and the recovery could reach more than 73%.

CAS / MDL: 4478-93-7
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TOXICOLOGY · 2020 · IF 4.099

Inhibition of ferroptosis attenuates busulfan-induced oligospermia in mice

Xi Zhao,Zhenhua Liu,Jie Gao,Hu Li,Xiaorong Wang,Yinchuan Li,Fei Sun

Busulfan is commonly used for cancer chemotherapy, nevertheless it cause male infertility via damaging the germ cells. Therefore, the underlying mechanism should be explored. In the present study, we demonstrated for the first time that ferroptosis was involved in busulfan-induced oligospermia in mice. Mice were given testicular injection of busulfan on both sides at the dose of 4 mg/kg body weight to establish the model of oligospermia. Four weeks later, the results showed that busulfan-treated mice exhibited decreased sperm concentration and motility, along with features of typical ferroptosis in testis, such as increased malondialdehyde (MDA) content and prostaglandin-endoperoxide synthase (PTGS2) mRNA expression, and decreased NADPH content. Inhibition of ferroptosis by ferrostatin-1 (Fer-1) or deferoxamine (DFO) partially alleviated busulfan-induced oligospermia in mice. Additionally, we also revealed that busulfan treatment induced spermatogenic cells ferroptosis by down-regulating nuclear factor-E2-related factor 2 (Nrf2) and glutathione peroxidase 4 (GPX4) expressions, and decreasing iron efflux through reduction of ferroportin 1 (FPN1) expression. Fer-1 or DFO obviously reversed busulfan-induced ferroptosis by increasing Nrf2, GPX4 and FPN1 expressions. Furthermore, after activation of Nrf2 by sulforaphane, sperm concentration and motility in busulfan-treated mice increased, accompanied by enhanced expressions of GPX4 and FPN1. These findings imply that busulfan-induced ferroptosis might be mediated via inhibition of Nrf2-GPX4 (FPN1) signaling pathway, and highlight that targeting ferroptosis serves as a potential strategy for prevention of busulfan-induced damage and male infertility.

CAS / MDL: 4478-93-7
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JOURNAL OF FOOD SCIENCE · 2024 ·Vol. 89 ·期 10 ·6707-6719 · IF 3.2

Sulforaphane nanoparticles coated with zein-propylene glycol alginate attenuate N-diethylnitrosamine-induced liver injury in mice

Qilei Wang,Zhenzhen Feng,Chan Shi,Xingang Lyu,DaiDi Fan

Sulforaphane-loaded nanoparticles (NP-SF) were prepared in this study to improve their biological effects. Based on propylene glycol alginate and zein as wall materials and anthocyanin and CaCl 2 as crosslinking agents, the NPs were encapsulated by the crosslinking method and freeze-dried. With the increasing contents of anthocyanin and Ca 2+ , the encapsulation efficiency and loading capacity of NP-SF were both increased. In vitro simulated digestion experiments showed controlled release of SF from the NPs. The pharmacokinetics confirmed that NP-SF exerted a slower release effect in rats, with improved SF bioavailability and protective effects on liver injury induced by N -diethylnitrosamine in mice. NP-SF reduced serum indicators of liver injury, increased the activities of antioxidant enzymes and GSH levels, and reduced malondialdehyde levels in the liver. In addition, SF activated the Keap1/Nrf2 signaling pathway and upregulated the expression of the Nrf2 downstream genes NQO1 and heme oxidase 1. High doses of NP-SF, in particular, had a higher therapeutic effect. In conclusion, encapsulation enhanced the biological activity of SF and promoted physiological function.

CAS / MDL: 4478-93-7 505-44-2
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Food Science and Human Wellness · 2024 · IF 5.6

Sulforaphane ameliorates non-alcoholic steatohepatitis by KLF4-mediated macrophage M2 polarization

Xianghui Huang,Jia Xu,Ye Xu,Bingxin Huangfu,Feng Zhang,Yanzhou Hu,Ruxin Gao,Xinxin Ren,Boyang Zhang,Kunlun Huang,Xiaoyun He

Non-alcoholic fatty liver disease (NAFLD) has become a global issue and a severe threat to public health. However, to date, no approved therapeutic drugs have been developed. Dietary interventions with natural products have shown promise in preventing and treating NAFLD. Sulforaphane (SFN) is a phytocompound with antioxidant and anti-inflammatory properties, and previous research has demonstrated that SFN can ameliorate hepatic lipid accumulation and inflammation. However, the molecular mechanisms underlying these beneficial effects remain unclear. In this study, we confirmed the protective effects of SFN on excessive lipid accumulation and inflammatory injury in a high-fat, high-fructose diet-induced non-alcoholic steatohepatitis (NASH) mouse model. We found that SFN attenuates the inflammatory injury in a macrophage cell line and the liver of NASH mice, owing to the promotion of M1-type macrophage polarization toward the M2-type and the regulation of inflammatory mediators. Further analysis demonstrated that this SFN-induced macrophage M2-type polarization occurs in a Krüppel-like factor 4 (KLF4)-dependent manner. In summary, we uncovered a new mechanism of action underlying SFN activity and provide evidence that dietary intervention with SFN might be protective against NASH.

CAS / MDL: 4478-93-7
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AQUACULTURE NUTRITION · 2025 ·Vol. 2025 ·期 1 ·6665220 · IF 3.9

Sulforaphane Repairs Oxidative Stress Damage Induced by Oxidized Fish Oil by Activating Nrf2 in Litopenaeus vannamei

Shiping Yang,Leyuan Feng,Junliang Luo,Jichang Jian,Shuanghu Cai,Huiling Liu

Nuclear factor erythroid 2-related factor 2 (Nrf2) is an essential component in regulating oxidative stress. Sulforaphane (SFN) is a natural antioxidant and gene Nrf2 agonist that can increase the antioxidant capacity of the organism and reduce oxidative stress. However, research on the repair of oxidative stress damage by SFN in aquatic animals remains extremely scarce. In order to further explore the function and role of SFN in the repair of oxidative stress injury in aquatic animals, this study took Litopenaeus vannamei as the research object. We established an oxidative stress model of L. vannamei through 6% oxidized fish oil (OFO) feeding. Methods, such as RNA interference (RNAi), qPCR, histopathological analysis, and TUNEL assay, were used to detect the changes in the oxidative stress status of L. vannamei . The results showed that the expression of Nrf2 in the hepatopancreas of L. vannamei in the double-stranded RNA (dsRNA)- Nrf2 + SFN group was significantly higher than that in the dsRNA- Nrf2 group and control group at 24 h ( p < 0.05). The transcription levels of antioxidant and autophagy genes in the SFN group were significantly higher than those in the control group ( p < 0.05), and the expression of related genes in the dsRNA- Nrf2 + SFN group was also higher than that in the dsRNA- Nrf2 group. Histopathology showed that Nrf2 knockdown would aggravate hepatopancreatic apoptosis and vacuolation, while SFN treatment after Nrf2 knockdown could alleviate hepatopancreatic injury and apoptosis caused by OFO. The results indicated that SFN could repair the oxidative stress injury of L. vannamei induced by OFO by activating Nrf2 . This study investigated the role of SFN in alleviating and repairing the oxidative stress damage in L. vannamei caused by OFO, aiming to provide a theoretical basis for the research on the antioxidant effect of SFN and the regulation of the antioxidant capacity of shrimp.

CAS / MDL: 4478-93-7
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES · 2025 ·Vol. 26 ·期 16 ·7791 · IF 4.9

Therapeutic Effects of Sulforaphane on Helicobacter pylori-Infected Mice: Insights from High-Coverage Metabolomics and Lipidomics Analyses of Serum and Liver

Shuling He,Lvyun Sun,Jiali Chen,Yixin Li,Ying Pan,Amei Su,Qiuyao Mao,Jiaqian Hu,Disheng Feng,Yang Ouyang

Sulforaphane, a natural isothiocyanate predominantly found in cruciferous vegetables, has shown potential in preventing and treating Helicobacter pylori infection. However, the underlying metabolic mechanisms remain largely unclear. This study employed high-coverage metabolomics and lipidomics methods to comprehensively investigate the effects of sulforaphane on the serum and liver metabolic profiles of H. pylori -infected mice. Metabolomics and lipidomics analysis revealed that H. pylori infection disrupted multiple metabolic pathways, leading to perturbations in amino acids, fatty acids, bile acids, and various lipid species. Sulforaphane treatment can ameliorate these disruptions, notably reversing alterations in serum glycerophospholipids and restoring hepatic levels of amino acids, bile acids, glycerophospholipids, ceramides, and peptides. Key metabolic pathways implicated included glutathione metabolism and glycine and serine metabolism, which are associated with antioxidant defense and host resistance to pathogenic infections. These findings offer a comprehensive metabolic basis for understanding the therapeutic effects of sulforaphane against H. pylori infection.

CAS / MDL: 4478-93-7
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