查找使用阿拉丁产品的科研文献

Apios americana Medik leaf extracts attenuate H2O2-induced hepatotoxicity

Qiang Chu,Ruoyi Jia,Chaowei Chen,Yaxuan Wang,Xin Yu,Yiru Zhang,Tao Wu,Xiaodong Zheng

Apios americana Medik leaves are rich in polyphenols and prevent glucose-induced damage in organisms. Polyphenols are a group of natural antioxidants. Therefore, a H 2 O 2 induced oxidative stress model of HepG2 cells was used to explore the protective effects of the Apios americana Medik leaves water extract (ALWE) against oxidative stress. Nine compounds were identified in ALWE using HPLC-TOF-MS including C 18 H 24 O 13 , which had not previously been reported. Fluorescence staining assays showed that the ALWE significantly decreased apoptosis, intracellular ROS generation, mitochondrial membrane potential (MMP) dissipation and mitochondrial membrane lipid peroxidation after ALWE pretreatment. Data from western blots showed that Keap1-Nrf2 and Sirt1-FoxO1 signaling pathways were involved in preventing H 2 O 2 induced oxidative stress. Transmission electron microscope and Western blot analyses indicated that autophagy contributed to the regulation of the oxidative balance. These results together indicated that ALWE is a potential antioxidant and autophagy activator, and it protects HepG2 cells against H 2 O 2 damage through activation of autophagy.

Four Different Structural Dietary Polyphenols, Especially Dihydromyricetin, Possess Superior Protective Effect on Ethanol-Induced ICE-6 and AML-12 Cytotoxicity: The Role of CYP2E1 and Keap1-Nrf2 Pathways

Wan Wang,Hang Shang,Jinzhe Li,Yue Ma,Cong Xu,Jiage Ma,Juncai Hou,Zhanmei Jiang

Polyphenols have received attention as dietary supplements for the relief of alcoholic liver disease (ALD) due to various bioactivities. Ethanol-induced rat small intestinal epithelial cell 6 (IEC-6) and alpha mouse liver 12 (AML-12) cell models were pretreated with four dietary polyphenols with different structures to explore their effects on cytotoxicity and potential protective mechanisms. The results showed that polyphenols had potential functions to inhibit ethanol-induced AML-12 and IEC-6 cell damage and oxidative stress, and restore ethanol-induced IEC-6 permeability and tight junction gene expression. Especially, dihydromyricetin (DMY) had the best protective effect on ethanol-induced cytotoxicity, followed by apigenin (API). Western blot results showed that DMY and API had the best ability to inhibit CYP2E1 and Keap1, and promote nuclear translocation of Nrf2, which might be the potential mechanism by which DMY and API attenuate ethanol-induced cytotoxicity. Moreover, the molecular docking results predicted that DMY and API could bind more tightly to the amino acid residues of CYP2E1 and Keap1, which might be one of the inhibitory modes of dietary polyphenols on CYP2E1 and Keap1. This study provided a rationale for the subsequent protective effect of dietary polyphenols on alcohol-induced liver injury in animal models and provided new clues on bioactive components for ALD-protection based on the gut-liver axis.

Naringenin alleviates myocardial ischemia/reperfusion injury by regulating the nuclear factor-erythroid factor 2-related factor 2 (Nrf2) /System xc-/ glutathione peroxidase 4 (GPX4) axis to inhibit ferroptosis

Shujun Xu,Bingxin Wu,Biying Zhong,Luoqi Lin,Yining Ding,Xiao Jin,Zhiwei Huang,Miaoyang Lin,Huanlin Wu,Danping Xu

Ferroptosis is an important form of myocardial cell death in myocardial ischemia-reperfusion injury (MIRI). Naringenin (NAR), as a flavonoid, has a significant advantage in improving MIRI. But the regulatory effect and mechanism of NAR on ferroptosis in MIRI have not been reported. After the rats were given NAR and induced to form myocardial ischemia-reperfusion (MI/R) injury, Tetrazolium chloride (TTC) staining was used to detect the myocardial infarction area of rats, and Hematoxylin-eosin (H&E) staining was used to detect myocardial injury. The markers of tissue inflammation were detected by ELISA. Serum creatine kinase Serum creatin kinase (CPK), Lactate dehydrogenase (LDH), and lipid peroxide (LPO) and oxidative stress related levels were measured. In addition, iron detection kits were used to detect total iron and Fe2+ levels in cardiac tissues, and western blot was used to detect the expression of ferroptosis-related proteins and the expression of nuclear factor-erythroid factor 2-related factor 2 (Nrf2) and glutathione peroxidase 4 (GPX4). At the cellular level, H9C2 cardiomyocytes were induced by hypoxia/reoxygenation (H/R), and ferroptosis inducer Erastin was administered to detect cell viability, ferroptosis-related indicators, oxidative stress related indicators, and expressions of Nrf2 and GPX4, to explore the mechanisms involved. NAR alleviated MI/R-induced pathological damage, inflammation and lipid peroxidation in myocardial tissue of rats. NAR adjusted the NRF2 /System xc – /GPX4 axis and improved ferroptosis. At the cellular level, ferroptosis inducer Erastin reversed the protective effect of NAR on H/R-induced H9C2 cardiomyocytes. In conclusion, NAR can alleviate MIRI by regulating the Nrf2/System xc-/GPX4 axis to inhibit ferroptosis.

UVA-responsive Fe₃O₄@ZnO nanocarrier grafted with anti-EGFR antibody for precision delivery of Nrf2-siRNA and brusatol: A novel platform for integrated photodynamic, gene, and chemotherapy

Qian Ren,Tingting Tian,Bin Wang,Jun Pan,Yong Huang,Li Zhong,Yehong Wang,Xia Wang,Xiao Huang

Photodynamic therapy (PDT) remains underutilized as a primary cancer treatment due to the limited lethality of reactive oxygen species (ROS) and poor targeting efficiency of traditional photosensitizers. This the aim of the study is to develop a Fe₃O₄@ZnO nanoparticle photosensitizer co-loaded with anti-EGFR antibody, brusatol, and Nrf2-siRNA to improve the therapeutic effect of PDT. This system can be guided to tumors by a magnetic field and further targets cancer cells through EGFR-specific binding. Under UVA light, brusatol and Nrf2-siRNA are released, enabling combined chemo-, gene, and photodynamic therapy. With the photosensitizer treatment, ROS levels in cutaneous squamous cell carcinoma cells were elevated by 191.09 ± 10.02 % through suppression of Nrf2 and its associated antioxidant defenses, significantly enhancing cell lethality and reducing cell viability by 80.43 ± 9.37 %. In vivo studies further demonstrated a tumor suppression rate of 76.30 ± 5.12 % in nude mice, highlighting the robust anti-tumor efficacy of the photosensitizer and its potential for clinical application in targeted cancer therapy. The biocompatibility and high therapeutic efficacy of this photosensitizer highlight its promise as a safer and more effective option for treating cutaneous squamous cell carcinoma.

Alleviation effect of arabinogalactan on decabromodiphenyl ether (BDE-209)-stimulated intestinal epithelial barrier damage via the Nrf2/HO-1/NQO1 signaling pathway in a Caco-2 cell monolayer model

Shaoying Gong,Jiachen Zheng,Lin Wang,Ruoyu Wu,Jianchun Han,Yongxin She

Decabromodiphenyl ether (BDE-209), a widely used polybrominated diphenyl ether, is a persistent environmental pollutant with intestinal toxicity. Arabinogalactan possesses antioxidant and anti-inflammatory properties, but its ability to counteract BDE-209-induced intestinal epithelial barrier (IEB) damage remains unclear. This study examined the protective effects of arabinogalactan on BDE-209-induced IEB damage and the underlying mechanisms. Arabinogalactan significantly restored barrier integrity, as evidenced by increased transepithelial electrical resistance and reduced FITC-dextran permeability. Mechanistically, it attenuated oxidative stress by regulating the levels of reactive oxygen species, glutathione, and malonaldehyde and the activity of superoxide dismutase and reducing the secretion of inflammatory cytokines (IL-1β, IL-6, and TNF-α). Arabinogalactan also preserved tight junction protein expression (claudin-1, zonula occludens [ZO]-1, occludin), lowered intracellular Ca²⁺, and activated the Nrf2/HO-1/NQO1 pathway. Taken together, these findings suggest that arabinogalactan inhibits oxidative stress and inflammation by regulating the Nrf2/NQO1/HO-1 signaling pathway to upregulate TJ expression, thereby alleviating BDE-209-induced IEB damage.

Muscle-Targeted Nanocomposite Therapy Alleviates Age-Related Sarcopenia via Antioxidant and Metabolic Reprogramming

Zhang Liu,Zile Shen,Hengli Lu,Bingqiang Lu,Peng Zhang,Wenhao Chen,Guowei Huang,Xinyu Qu,Zhen Yu,Feng Chen,Wangfu Zang

Sarcopenia, a progressive skeletal muscle disorder marked by loss of mass and function, presents growing societal challenges due to limited therapeutic options. Here, we identify mitochondrial dysfunction and oxidative stress as central drivers of sarcopenia through integrated bioinformatics and clinical validation. To address this pathophysiology, we engineer a muscle-targeted nanocomposite (BP-PEG-MOTS-c, BM) combining mitochondrial-derived peptide MOTS-c with antioxidant black phosphorus nanosheets (BP). BM exhibits dual functionality: MOTS-c restores mitochondrial function, while BP synergistically amplifies ROS scavenging capacity. In cellular and murine models with age-related sarcopenia, BM treatment alleviates muscle dysfunction and muscle loss, concurrently normalizing mitochondrial function and reducing lipid peroxidation. Mechanistic profiling via RNA-seq reveals BM’s activation of PI3K/AKT/Nrf2 and suppression of ROS/p38 MAPK signaling pathway, mediating antioxidant responses and maintenance of mitochondrial homeostasis. The nanocomposite demonstrats superior biocompatibility in toxicity assays, outperforming conventional delivery systems. Our findings establish that BM has been established as a promising mitochondrial redox modulator with translational potential for sarcopenia and related age-associated pathologies.

Biomimetic fucoidan nanoparticles with regulation of macrophage polarization for targeted therapy of acute lung injury

Weili Yang,Hui Liu,Xiaowei Liu,Yuxin Cao,Xuemei Wang,Xinxin Wang,Wenwen Cao,Chunjing Guo,Daquan Chen

Acute lung injury (ALI) is a complex acute respiratory illness with a high mortality rate. Reactive oxygen species (ROS) play a pivotal role in ALI, inducing cellular damage, inflammation, and oxidative stress, thereby exacerbating the severity of the injury. In this study, inspired by the “subtractive” strategy, we developed a fucoidan-based macrophage membrane bio-nanosystem, abbreviated as MF@CB, designed as an anti-inflammatory and antioxidant agent to alleviate lipopolysaccharide (LPS)-induced inflammation in ALI. MF@CB coated with macrophage membrane for effective targeting and accumulation in ALI lesions. In addition, MF@CB activates Nrf2 transcriptional activity in macrophages, inhibiting ROS synthesis at its origin while effectively removing ROS already present in the ALI. This dual-pronged approach demonstrates robust antioxidant properties and restores the macrophage antioxidant defense barrier. In the LPS-induced ALI mouse model, MF@CB significantly mitigated lung inflammatory damage by modulating lung macrophage polarization and inhibiting the over-secretion of pro-inflammatory cytokines by activated immune cells. More importantly, unlike most surface modification strategies because it remove the molecule, this approach is easier to apply and potentially safer and may provide useful insights into the development of more effective therapeutic strategies for ALI.

Atraric acid alleviates high-fat diet-induced renal injury, lipid accumulation, and fibrosis in mice by regulating oxidative stress and inflammation through AMPK-dependent Nrf2 and NF-κB signaling pathways

Yannan Xiang,Tianyue Guan,Jun Wang,Shasha Zhang,Yusa Li,Jing Xia,Panpan Zhao,Lei Wang

This study explores the protective effects of Atraric Acid (AA) against chronic kidney disease (CKD) induced by a high-fat diet (HFD) and its underlying mechanisms. In vivo HFD-induced CKD mouse models and in vitro OA/PA-stimulated HK2 cells were treated with AA. AA improved kidney morphology, reduced fibrosis, lipid accumulation, and body weight. It also decreased serum TC, TG, HDL-C, Scr, BUN, and Cys-C levels, indicating improved renal function. AA alleviated oxidative stress, ROS accumulation, and inflammation, as confirmed by DHE staining, oxidative stress markers, and pro-inflammatory cytokine levels. Western blotting showed that AA activated Nrf2 and suppressed NF-κB signaling. AMPK inhibition experiments demonstrated that AA regulated Nrf2 and NF-κB via AMPKα phosphorylation. In conclusion, AA mitigates HFD-induced CKD by targeting AMPKα to regulate oxidative stress and inflammation.

The ameliorating effects of Guizhi Fuling Wan combined with rosiglitazone in a rat ovarian model of polycystic ovary syndrome by the PI3K/AKT/NF-κB and Nrf2/HO-1 pathways

Yongju Ye,Weimei Zhou,Yuefang Ren,Jiali Lu,Aixue Chen,Ruiying Jin,Feilan Xuan

Fresh Dendrobium Officinale Polysaccharides Combine with Penicillamine to Attenuate Copper Overload-Induced Liver Injury in a Rat Model of Wilson’s Disease Via Activation of the Nrf2/HO-1/Keap1 Signaling Pathway

Zhang Shenao,Liu Pangwei,Jiang Yuge,Wu Huan,Cao Shijian,Xuan Shujuan,Wu Hongfei,Zhou An

Wilson’s disease (WD) is characterized by pathological copper accumulation, which drives hepatocellular oxidative stress and subsequent liver injury. While the first-line chelator penicillamine (PCA) effectively eliminates copper, it is associated with significant side effects. Dendrobium officinale polysaccharides, the active components in Dendrobium officinale , exhibit significant antioxidant and hepatoprotective effects. However, their potential in ameliorating liver injury in WD and as an adjunctive therapy to PCA remains unclear. This study investigated the hepatoprotective effects and underlying mechanisms of fresh Dendrobium officinale polysaccharides (FDOP), both alone and combined with PCA, in a copper-overloaded rat model. The results showed that FDOP significantly mitigated hepatic histopathological damage and reduced serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (AKP). It also alleviated oxidative stress by decreasing hepatic malondialdehyde (MDA) and oxidized glutathione (GSSG) levels while enhancing superoxide dismutase (SOD) activity. Furthermore, FDOP promoted copper excretion and reduced copper deposition in the liver, brain, and kidneys. Mechanistically, FDOP activated the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1)/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway, evidenced by upregulated nuclear Nrf2 and HO-1 expression and downregulated Keap1 expression, thereby enhancing the cellular antioxidant defense system. Importantly, the combination of FDOP and PCA outperformed either monotherapy in alleviating liver injury, promoting copper excretion, and activating antioxidant pathways. In conclusion, FDOP not only exhibits excellent hepatoprotective effects but also holds potential as an adjunct to PCA therapy, offering a novel combined treatment strategy for WD.

Lycii Fructus, a medicine food homology material, attenuates retinal damage in sodium iodate-induced retinal degeneration mice and inhibits oxidation-induced apoptosis of Müller cells via regulating Nrf2-HO1 signaling pathway

Cheng Cao,Yunqing Lu,Bing Li,Yang Chen,Pan Xu,Mengqiu Liu,Ziqiang Zhu,Lei Yuan,Sheng Guo,Hongjie Kang,Jin-ao Duan,Yue Zhu

Lycii Fructus (LF) is a medicinal-edible homology material frequently used for treating age-related macular degeneration (AMD) in Chinese medicine. Abundant of literatures verified the retina protection effect of LF on AMD-like animal models. However, previous studies on LF attenuating retinal damage mainly focused on its protection effect on pigment epithelial cells and optic ganglion cells while few reports on Müller cells. In the current study, we found that LF extracts attenuated oxidation damages and inhibited cell apoptosis of retina on a mouse retinal injury model induced by sodium iodate. LF extracts also increased expressions of Müller cell biomarker glutamine synthetase of eyeballs of model mice, which indicated that LF extract protected Müller cell from oxidation injury induced by sodium iodate. In Müller cell MIO-M1 cultures, LF also significantly inhibited cellular apoptosis induced by NaIO 3 by regulating Nrf2/HO-1 signaling pathway and the aqueous extracts exerted better active tendency than ethanol extracts. These data implied that the antioxidant effect of LF on protecting Müller cell might contribute to its retina repair function, thereby providing more scientific evidences for the development of LF as an alternative therapy or preventive measures for AMD.

Purified Tetrastigma hemsleyanum vines polysaccharide attenuates EC-induced toxicity in Caco-2 cells and Caenorhabditis elegans via DAF-16/FOXO pathway

Qiang Chu,Ruoyi Jia,Wen Chen,Yangyang Liu,Yonglu Li,Xiang Ye,Yong Jiang,Xiaodong Zheng

Ethyl Carbamate (EC), as a carcinogen widely found in fermented foods, was verified that its cytotoxicity was associated with oxidative stress. Polysaccharides from natural sources due to their antioxidative capacity have attracted great attention in the past time. In this study, purified polysaccharide from Tetrastigma hemsleyanum vines (TVP) with 64.89 kDA was extracted and conducted multiple analysis to identify its structural information. It could be discovered that TVP was composed of mannose, rhamnose, glucuronic acid, glucose, galactose, and arabinose. In vitro , TVP could inhibit cytotoxicity and genotoxicity, attenuate oxidative damage and mitochondrial dysfunction induced by EC in Caco-2 cells. Meanwhile, TVP could suppress apoptosis by mTOR and Bcl-2 signaling pathways, ameliorate oxidative via Sirt1-FoxO1 and Nrf2-Keap1 signaling pathways. In vivo , EC as well triggered the decline of survival and athletic ability in Caenorhabditis elegans ( C. elegans ) and TVP could reverse the decline. In the meantime, TVP could ameliorate oxidative damage in N2 and daf-2 (-) mutant but fail in daf-16 (-) mutant, which suggested that DAF-16 (FOXO) might affect the antioxidative protection of TVP in C. elegans . In brief, our results manifested that TVP could attenuate EC-induced cytotoxicity both in vitro and in vivo .