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Experimental and Therapeutic Medicine · 2023 ·Vol. 25 ·期 5 ·1-7 · IF 2.7

The hepatoprotective effect of aspirin on carbon tetrachloride‑induced hepatic fibrosis via inhibition of TGFβ‑1 pathway and pro‑inflammatory cytokines IL‑1β and COX‑2 in rats

Zhiguo Wu,Yuchan Wu,Weicheng Zhong,Qingmei Zhong,Shengfang Rao,Dongshan Yu,Xiaolu Luo,Fang Qiu,Zhiying Song,Di Jin,Maoxing Ai,Yu Lan,Gongchang Zhang,Shufeng Song,Baogang Xie,Shuilin Sun

Aspirin decreases liver fibrosis index and inflammation levels. However, the exact mechanism underlying the effects of aspirin are yet to be elucidated. The aim of the study was to investigate the potential protective effects of aspirin on carbon tetrachloride (CCl4)‑induced hepatic fibrosis in Sprague‑Dawley rats. Rats were divided into four groups, including healthy and CCl4 control and low‑(aspirin 10 mg/kg + CCl4) and high‑dose aspirin group (aspirin 300 mg/kg + CCl4). After 8 weeks treatment, the histopathological examinations of hepatocyte fibrosis in liver and serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), IL‑1β, transforming growth factor‑β1 (TGF‑β1), hyaluronic acid (HA), laminin (LN) and type IV collagen (IV.C) were determined. Histopathological examination suggested that aspirin decreased CCl4‑induced hepatic fibrosis and liver inflammation. The high‑dose aspirin group significantly decreased the serum levels of ALT, AST, HA and LN compared with the CCl4 control group. High‑dose aspirin group significantly decreased the levels of pro‑inflammatory cytokines IL‑1β compared with CCl4 group. The high‑dose aspirin group significantly inhibited the expression of TGFβ‑1 protein compared with CCl4 group. Overall, the present study indicated that aspirin exhibited potent protective effects against CCl4‑induced hepatic fibrosis via inhibition of the TGFβ‑1 pathway and pro‑inflammatory cytokine IL‑1β.

CAS / MDL: 329-98-6
研究领域: 药理学 · 肝病学 · 炎症 · 纤维化 · 细胞因子
✓ 已验证 产品关联 DOI PubMed 高影响因子
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JOURNAL OF ETHNOPHARMACOLOGY · 2024 · IF 4.8

Desmodium styracifolium (Osb.) Merr. extracts alleviate cholestatic liver disease by FXR pathway

Zhiyuan Zhang,Guoqiang Guan,Zixuan Tang,Weimin Wan,Zhipeng Huang,Yuefeng Wang,Jianzhao Wu,Bo Li,Mingli Zhong,Kefeng Zhang,Lixian Nong,Ya Gao,Houkang Cao

A B S T R A C T Ethnopharmacological relevance Cholestatic liver disease (CLD) is a disease characterized by cholestasis. Farnesoid X receptor (FXR) is a nuclear receptor that maintains homeostasis in bile acid metabolism. Studies have shown that gut microbiota interfered with the FXR pathway. Modulation of FXR to inhibit cholestasis has become a key measure in the treatment of CLD. In traditional folk medicine, Desmodium styracifolium (Osb.) Merr. was used as a primary treatment for gallstones, gonorrhea, jaundice, cholecystitis and other diseases. Modern pharmacological studies had also found that the herb has anti-calculus, anti-inflammatory, antioxidant, diuretic and liver damage. Therefore, we speculated that Desmodium styracifolium (Osb.) Merr. extracts (DME) could alleviate CLD through the FXR pathway and might be associated with the gut microbiota. However, studies of DME alleviating CLD through the FXR pathway have not been reported. Aim of study To study the effect and mechanism of DME in relieving CLD through in vivo and in vitro experiments. Materials and methods First, mice were administrated with alpha-naphthyl isothiocyanate (ANIT) to establish a CLD model in vivo . Meanwhile, HepG2 cells were induced by lithocholic acid (LCA) to establish the CLD model in vitro . To evaluate the therapeutic effect of DME on CLD mice, hematoxylin-eosin (HE) staining, and biochemical indicators were performed. The prototype of the blood components in mice serum was detected by ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). 16S rDNA sequencing was used to analyze the gut microbiota. Finally, the protein and mRNA expression of the FXR pathway in mice liver tissues or HepG2 cells were detected by Western blot, qRT-PCR, or immunofluorescence. Results Pathological testing and biochemical indexes showed that DME significantly reduced serum ALT, AST, ALP, TBIL, DBIL, TBA and liver TBA levels, and attenuated liver tissue injury, necrosis and jaundice in CLD mice. In addition, MetagenomeSeq analysis of gut microbiota showed that DME significantly up-regulated the abundance of Parvibacter , down-regulated the abundance of Paenalcaligenes , and regulated bile acid homeostasis. In terms of mRNA expression, DME significantly upregulated the mRNA levels of Nr1h4, Abcb11, Cyp7a1 and Slc10a1. Meanwhile, in terms of protein expression, DME significantly up-regulated the protein expression levels of FXR, BSEP, CYP7A1 and NTCP, which regulated bile acid homeostasis. Finally, the molecular docking results showed that the components of DME, such as Lumichrome, Daidzein and Folic acid, all had good binding ability with FXR, and the surface plasmon resonance (SPR) results also showed that both Lumichrome and Daidzein had a relatively high affinity with FXR. Conclusion DME alleviated CLD through the FXR pathway, and the mechanisms might be associated with the gut microbiota.

研究领域: 药理学 · 肝病学 · 分子生物学 · 微生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY · 2019 · IF 3.571

Coumarin Analogues from the Citrus grandis (L.) Osbeck and Their Hepatoprotective Activity

Danmei Tian,Fangfang Wang,Menglong Duan,Lingyun Cao,Youwei Zhang,Xinsheng Yao,Jinshan Tang

Seven new coumarin analogues (1, 2, and 4–8), together with ten known analogues (3, 9–17), were isolated from the air-dried pericarp of Citrus grandis. The structures of these compounds were determined by HR-ESI-MS, UV/vis, and 1D- and 2D-NMR spectra. Meanwhile, the hepatoprotective activities of all these coumarins were evaluated by MTT assays using the d-galactosamine-induced LO2 cell injury model. The results show that compounds 3 and 4 exhibited the strongest hepatoprotective activities. Moreover, compounds 3 and 4 suppressed increases in the levels of alanine transaminase (ALT) and aspartate transaminase (AST) in d-galactosamine-treated LO2 cells, further confirming the hepatoprotective effects of these compounds. Mechanistically, compounds 3 and 4 increased the activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased the level of malondialdehyde (MDA) in injured LO2 cells induced by d-galactosamine. These findings shed light on a better understanding of the hepatoprotective effect of Citrus grandis, providing novel insights into the development of coumarin-based hepatoprotective drugs in the future.

研究领域: 药理学 · 天然产物化学 · 肝病学
✓ 已验证 DOI PubMed 高影响因子
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JOURNAL OF ETHNOPHARMACOLOGY · 2024 · IF 4.8

Mechanistic studies on the alleviation of ANIT-induced cholestatic liver injury by Polygala fallax Hemsl. polysaccharides

Guoqiang Guan,Houkang Cao,Zixuan Tang,Kefeng Zhang,Mingli Zhong,Rui Lv,Weimin Wan,Fengyue Guo,Yongwang Wang,Ya Gao

Ethnopharmacological relevance Polygala fallax Hemsl. is a traditional folk medicine commonly used by ethnic minorities in the Guangxi Zhuang Autonomous Region, and has a traditional application in the treatment of liver disease. Polygala fallax Hemsl . polysaccharides (PFPs) are of interest for their potential health benefits. Aim of this study This study explored the impact of PFPs on a mouse model of cholestatic liver injury (CLI) induced by alpha-naphthyl isothiocyanate (ANIT), as well as the potential mechanisms. Materials and methods A mouse CLI model was constructed using ANIT (80 mg/kg) and intervened with different doses of PFPs or ursodeoxycholic acid. Their serum biochemical indices, hepatic oxidative stress indices, and hepatic pathological characteristics were investigated. Then RNA sequencing was performed on liver tissues to identify differentially expressed genes and signaling pathways and to elucidate the mechanism of liver protection by PFPs. Finally, Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used to verify the differentially expressed genes. Results Data analyses showed that PFPs reduced the levels of liver function-related biochemical indices, such as ALT, AST, AKP, TBA, DBIL, and TBIL. PFPs up-regulated the activities of SOD and GSH, down-regulated the contents of MDA, inhibited the release of IL-1β, IL-6, and TNF-α, or promoted IL-10. Pathologic characterization of the liver revealed that PFPs reduced hepatocyte apoptosis or necrosis. The RNA sequencing indicated that the genes with differential expression were primarily enriched for the biosynthesis of primary bile acids, secretion or transportation of bile, the reactive oxygen species in chemical carcinogenesis, and the NF-kappa B signaling pathway. In addition, the results of qRT-PCR and Western blotting analysis were consistent with those of RNA sequencing analysis. Conclusions In summary, this study showed that PFPs improved intrahepatic cholestasis and alleviated liver damage through the modulation of primary bile acid production, Control of protein expression related to bile secretion or transportation, decrease in inflammatory reactions, and inhibition of oxidative pressure. As a result, PFPs might offer a hopeful ethnic dietary approach for managing intrahepatic cholestasis.

CAS / MDL: 128-13-2 551-06-4
研究领域: 药理学 · 分子生物学 · 肝病学 · 民族药理学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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ANALYTICAL CHEMISTRY · 2024 · IF 6.7

Machine Learning Assisted MALDI Mass Spectrometry for Rapid Antimicrobial Resistance Prediction in Clinicals

Weibo Gao,Hang Li,Jingxian Yang,Jinming Zhang,Rongxin Fu,Jiaxi Peng,Yechen Hu,Yitong Liu,Yingshi Wang,Shuang Li,Shuailong Zhang

Antimicrobial susceptibility testing (AST) plays a critical role in assessing the resistance of individual microbial isolates and determining appropriate antimicrobial therapeutics in a timely manner. However, conventional AST normally takes up to 72 h for obtaining the results. In healthcare facilities, the global distribution of vancomycin-resistant Enterococcus fecium (VRE) infections underscores the importance of rapidly determining VRE isolates. Here, we developed an integrated antimicrobial resistance (AMR) screening strategy by combining matrix-assisted laser desorption ionization mass spectrometry (MALDI-MS) with machine learning to rapidly predict VRE from clinical samples. Over 400 VRE and vancomycin-susceptible E. faecium (VSE) isolates were analyzed using MALDI-MS at different culture times, and a comprehensive dataset comprising 2388 mass spectra was generated. Algorithms including the support vector machine (SVM), SVM with L1-norm, logistic regression, and multilayer perceptron (MLP) were utilized to train the classification model. Validation on a panel of clinical samples (external patients) resulted in a prediction accuracy of 78.07%, 80.26%, 78.95%, and 80.54% for each algorithm, respectively, all with an AUROC above 0.80. Furthermore, a total of 33 mass regions were recognized as influential features and elucidated, contributing to the differences between VRE and VSE through the Shapley value and accuracy, while tandem mass spectrometry was employed to identify the specific peaks among them. Certain ribosomal proteins, such as A0A133N352 and R2Q455, were tentatively identified. Overall, the integration of machine learning with MALDI-MS has enabled the rapid determination of bacterial antibiotic resistance, greatly expediting the usage of appropriate antibiotics.

研究领域: 临床微生物学 · 质谱学 · 机器学习 · 抗菌耐药性 · 医学信息学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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TOXICOLOGY AND APPLIED PHARMACOLOGY · 2018 · IF 3.616

Emodin-induced hepatotoxicity was exacerbated by probenecid through inhibiting UGTs and MRP2

Lili Wu,Yulian Chen,Han Liu,Zhikun Zhan,Zhi Liang,Tao Zhang,Zheng Cai,Ling Ye,Menghua Liu,Jie Zhao,Shuwen Liu,Lan Tang

Aggravating effect of probenecid (a traditional anti-gout agent) on emodin-induced hepatotoxicity was evaluated in this study. 33.3% rats died in combination group, while no death was observed in rats treated with emodin alone or probenecid alone, indicating that emodin-induced (150 mg/kg) hepatotoxicity was exacerbated by probenecid (100 mg/kg). In toxicokinetics-toxicodynamics (TK-TD) study, aspartate aminotransferase (AST) and systemic exposure (area under the serum concentration-time curve, AUC ) of emodin and its glucuronide were significantly increased in rats after co-administrated with emodin and probenecid for 28 consecutive days. Results showed that the increased AUC (increased by 85.9%) of emodin was mainly caused by the decreased enzyme activity of UDP-glucuronosyltransferases (UGTs, decreased by 11.8%–58.1%). In addition, AUC of emodin glucuronide was increased 5-fold, which was attributed to the decrease of multidrug-resistant-protein 2 (MRP2) protein levels (decreased by 54.4%). Similarly, in vitro experiments proved that probenecid reduced the cell viability of emodin-treated HepG2 cells through inhibiting UGT1A9, UGT2B7 and MRP2. Our findings demonstrated that emodin-induced hepatoxicity was exacerbated by probenecid through inhibition of UGTs and MRP2 in vivo and in vitro , indicating that gout patients should avoid taking emodin-containing preparations in combination with probenecid for a long time.

研究领域: 药理学 · 毒理学 · 药学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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FITOTERAPIA · 2024 · IF 2.5

Kakuol and asarinin protecting liver injury via HSP90AA1/CDK2/mTOR signaling pathway

Ling Jiang,Cai-Bo Tian,Rui-Han Ye,Nian Shi,Xing-Chao He,Yun-Li Zhao,Xiao-Dong Luo

Drug-induced liver injury caused acute hepatic failure and hepatitis frequently. In this investigation, kakuol and asarinin reduced the levels of serum alanine transaminase (ALT), aspartate transaminase (AST) and malondialdehyde (MDA) dramatically, and ameliorated the pathological damage of liver tissues in APAP-induced mice. Furthermore, both compounds increased the viabilities of APAP-induced L-O2 cells and extracellular glutathione (GSH) levels accompanied significantly by reducing the level of intracellular ROS in vitro . In addition, HSP90AA1/CDK2/mTOR signaling pathway and five target proteins (CDK2, HSP90AA1, HRAS, MMP1, mTOR) were proposed from network pharmacology and molecular docking prediction, and then the up-regulation of protein expression of CDK2, mTOR and down-regulation of HSP90AA1, HRAS, MMP1 by kakuol and asarinin in western blotting supported their mechanism.

CAS / MDL: 103-90-2 22888-70-6
研究领域: 药理学 · 分子生物学 · 毒理学 · 肝病学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Chinese Herbal Medicines · 2019 · IF 0

Gynura procumbens aqueous extract alleviates nonalcoholic steatohepatitis through CFLAR-JNK pathway in vivo and in vitro

Ya-yun Liu,Jiao-jiao You,Wei Xu,Ting Zhai,Chun-yuan Du,Yong Chen,Feng-mei Han

Objective The present work was to investigate the protective effects of the aqueous extract of Gynura procumbens (GPAE) against nonalcoholic steatohepatitis (NASH) in mice and NCTC-1469 cells. Methods C57BL/6J mice were fed with methionine and choline-deficient (MCD) diet and administered simultaneously with GPAE (500 and 1000 mg/kg/d, respectively) by gavage for six weeks. The biomarkers of NASH in serum and liver were determined. NCTC-1469 cells were pretreated with 0.25 mmol/L palmitic acid (PA) plus 0.5 mmol/L oleic acid (OA) for 24 h or treated with adenovirus expressing short-hairpin RNA against CFLAR (Ad-shCFLAR) for 24 h and then treated with GPAE (80 and 160 µg/mL, respectively) for 24 h, and the content of cellular biomarkers of NASH was detected. Results In mice treated with MCD , GPAE could decrease the levels of serum ALT , AST, the content of hepatic TG , TC and MDA , repress the activities and protein expression of CYP2E1 and CYP4A and the phosphorylation of JNK, increase the activities of HO-1, CAT and GSH-Px, up-regulate the mRNA expression of PPARα, FABP5, CPT1α, ACOX, SCD-1, mGPAT, MTTP and the protein expression of CFLAR and NRF2. In NCTC-1469 cells treated with PA and OA, GPAE could decrease the content of cellular TG and ROS , promote the uptake of 2-NBDG, up-regulate the protein expression of CFLAR and NRF2. In NCTC-1469 cells treated with Ad-sh CFLAR , GPAE up-regulated the mRNA and protein expression of CFLAR, down-regulated the phosphorylation of JNK, and increased the protein expression of NRF2 and pIRS1 . Conclusion These results indicated that the activation on CFLAR-JNK pathway might be the main anti-NASH mechanism of GPAE, which on the one hand promote the β-oxidation and efflux of fatty acids in liver, and finally reduce hepatic lipid accumulation , on the other hand increase the activities of anti-oxidant enzymes and inhibit the activities of ROS generation enzymes by activating NRF2, and therefore attenuates hepatic oxidative stress damage.

CAS / MDL: 112-80-1
研究领域: 药理学 · 肝病学 · 分子生物学
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JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE · 2022 ·Vol. 103 ·期 4 ·2196-2206 · IF 4.125

Extraction, purification, structural characterization, and hepatoprotective effect of the polysaccharide from purple sweet potato

Chenjing Li,Yihua Feng,Jingyao Li,Rui Lian,Liehao Qin,Chunling Wang

BACKGROUND Purple sweet potato Ipomoea batatas (L.) has long been used as a medicine and a food. It contains various bioactive substances such as polysaccharides, anthocyanins, and flavonoids. Purple sweet potato polysaccharides are known to have anti-oxidant, anti-tumor, and immunomodulatory functions. Nevertheless, studies on the structural characterization of purple sweet potato polysaccharides and their ability to prevent non-alcoholic fatty liver disease (NAFLD) have rarely been reported. RESULTS A novel polysaccharide (PSPP-A) was extracted and isolated from purple sweet potato, and its structural characteristics and preventive effects on NAFLD were investigated. The results indicated that PSPP-A was composed of l -rhamnose, d -arabinose, d -galactose, d -glucose, and d -glucuronic acid with molar ratios of 1.89:8.45:1.95:1.13:1. Its molecular weight was 2.63 × 10 3 kDa. Methylation and nuclear magnetic resonance (NMR) analysis indicated that the glycosidic linkages were →3)- α -L-Ara f -(1→, α -L-Ara f -(1→, →2,4)- α -L-Rha p -(1→, 4-O-Me- β -D-GlcA p -(1→, →4)- α -D-Glc p -(1→, →4)- β -D-Gal p -(1→, and →6)- β -D-Gal p -(1→. Scanning electron microscopy (SEM) indicated that the structure of PSPP-A was irregular. Subsequently, the protective effect of PSPP-A on NAFLD was investigated. The results indicated that bodyweight, liver index, and triglyceride (TG), total cholesterol (TC), aspartate transaminase (AST), and alanine transaminase (ALT) content were significantly reduced by intervention of purple sweet potato polysaccharide-A (PSPP-A) compared with the - high-fat diet group. Liver histopathological analysis indicated that PSPP-A attenuated irregular hepatocyte patterns and excessive lipid vacuoles. CONCLUSIONS The novel polysaccharide, PSPP-A, mainly contains arabinose, which has certain preventive effects on NAFLD. This study provides a theoretical basis for further elucidating the hepatoprotective effect of purple sweet potatoes as a functional food. © 2022 Society of Chemical Industry.

研究领域: 食品科学 · 药理学 · 生物化学 · 营养学 · 医学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Food & Function · 2022 ·Vol. 13 ·期 16 ·8593-8604 · IF 6.317

Hepatoprotective effects of different mulberry leaf extracts against acute liver injury in rats by alleviating oxidative stress and inflammatory response

Yanfang Yu,Yuhuan Chen,Xuping Shi,Chuan Ye,Junwen Wang,Jinzhi Huang,Bing Zhang,Zeyuan Deng

This study investigated the hepatoprotective effects of various mulberry (Morus alba L.) leaf extracts (MLEs), including mulberry ethanol extract (MEE), aqueous extract (MAE) and a combination extract (MCE) against D-galactosamine (D-GalN)/lipopolysaccharide (LPS)-induced acute liver injury in rats. It aimed to explore the possible molecular mechanism of the liver-protecting function of mulberry leaves and provide a reference for choosing the appropriate extraction method. The results showed that the three extracts contained different amounts of phenolic compounds, 1-deoxynojirimycin (DNJ) and polysaccharides. MLEs markedly improved the pathological status of rat liver tissue, decreased the levels of AST, ALT, TNF-α, IL-1β, IL-6 and MDA, while increased the levels of GSH, SOD and CAT in the D-GalN/LPS-treated rats at the same time. MEE, with the highest amount of total phenolics, exhibited the highest antioxidant activity corresponding to the protein expression level of Nrf2 and HO-1. MCE significantly suppressed the expression of apoptosis-related dot-like protein (ASC) and Caspase-1 and inhibited the phosphorylation of p38 MAPK and ERK1/2, thereby showing high anti-inflammatory activity. These results indicated that the active components from mulberry leaves protected rats against acute liver injury, attributed to a reduction in both oxidative stress and inflammatory response. The protective effect may be implicated in regulating the Nrf2, NLRP3 and MAPK signaling pathways.

CAS / MDL: 19130-96-2 1772-03-8
研究领域: 药理学 · 肝病学 · 生物化学 · 分子生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Parasites & Vectors · 2022 ·Vol. 15 ·期 1 ·1-12 · IF 4.047

Multiple biochemical indices and metabolomics of Clonorchis sinensis provide a novel interpretation of biomarkers

Qiu Yang-Yuan,Chang Qiao-Cheng,Gao Jun-Feng,Bao Ming-Jia,Luo Hai-Tao,Song Jin-Ho,Hong Sung-Jong,Mao Rui-Feng,Sun Yun-Yi,Chen Ying-Yu,Liu Ming-Yuan,Wang Chun-Ren,Liu Xiao-Lei

Background Clonorchiasis, an infectious disease caused by the liver fluke Clonorchis sinensis , may lead to the development of liver and gallbladder diseases, and even cholangiocarcinoma (CCA). However, the pathogenesis, host-pathogen interaction, and diagnostic markers for clonorchiasis remain unclear. Methods Eighteen rabbits were randomly divided into control group ( n  = 9) and C. sinensis -infected group ( n  = 9), and their plasma samples were collected at 7, 14, 28, and 63 days post-infection (dpi). Biochemical indices and metabolites in different infection periods were detected. A non-targeted ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) approach was employed to investigate the metabolic profiles of plasma in rabbits, and related metabolic pathways of differential metabolites and correlation between candidate biochemical indices and differential metabolites were analyzed. Finally, the candidate biomarkers were verified with human samples using a targeted metabolomics method. Results The result of biochemical indices indicated C. sinensis infection would affect the liver function biochemical indices, especially alanine aminotransferase, aspartate transaminase (AST), glutamyl transpeptidase (GGT), total bile acid, high-density lipoprotein, and cholinesterase. The metabonomic results showed that 58, 212, 23, and 21 differential metabolites were identified in different phases of the infection. Multivariate statistical analysis of differential metabolites revealed distinct metabolic signatures during different phases of infection, with most of these signatures being observed at 14 dpi, which mainly influences the amino acid metabolisms. For metabolites and biochemical indices, AST, GGT, hypoxanthine, l -pipecolic acid, and d -glucuronate represented potential noninvasive biomarkers for the diagnosis of C. sinensis ( P  < 0.05 and AUC > 0.8). Furthermore, GGT and d -glucuronate levels were positively correlated with the infection ( r (28) = 0.98, P  < 0.0001) and showed excellent diagnostic performance (AUC = 0.972; 95% confidence interval, 0.921 to 1.000). Conclusions The present results provide new insights into plasma metabolic changes in rabbits during C. sinensis infection, and the potential biomarker may be used for developing an effective method to diagnose clonorchiasis in the future. Graphical Abstract

研究领域: 寄生虫学 · 代谢组学 · 医学诊断 · 传染病
✓ 已验证 DOI PubMed 高影响因子
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JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY · 2024 · IF 4.5

Lipid peroxide-regulated nanoparticles prevent the progression of nonalcoholic steatohepatitis by reducing lipid deposition and eliminating oxidative-stress

Yuman Zhang,Yao Yu,Qi Wang,Wenjun Shi,Hanying Hu,Danqing Hou,Zhi Li

Non-alcoholic fatty liver disease (NAFLD) was a pathological syndrome characterized by excessive lipid deposition in the liver. Excessive lipid in the liver produced reactive oxygen species (ROS), the occurrence of oxidative stress and lipid peroxidation was accelerated, which aggravated liver function damage. Based on these, resveratrol, a natural antioxidan, was encapsulated in liposoluble interior by amphiphilic phosphatidylserine, and then self-assembled with chitosan oligosaccharide complexed with zinc ions to form Zn-Cos/Res@Ps nanoparticles. The size of the Zn-Cos/Res@Ps was about 168.57 ± 4.35 nm, and the zeta potential was about 17.45 ± 1.79 mV. Furthermore, Zn-Cos/Res@Ps could significantly inhibition of lipid deposition, decreased the contents of reactive oxygen species (ROS) and synergistically decreased the levels of malondialdehyde (MDA) in HepG2 cells. Zn-Cos/Res@Ps could also reduce the content of serum total cholesterol (TC), triglyceride (TG), aspartate aminotransferase (AST) and alanine aminotransferase (ALT), improved the liver injury and reduced the degree of liver fibrosis in mice. The Zn-Cos/Res@Ps group showed better results than the single-drug nanoparticle group. In conclusion, Zn-Cos/Res@Ps nanoparticles could effectively alleviate the disease progression by inhibiting oxidative stress and lipid peroxidation, promoted fatty acid catabolism, and effectively reverse and prevent the progress of nonalcoholic steatohepatitis.

研究领域: 纳米技术 · 药理学 · 肝病学 · 分子生物学
✓ 已验证 DOI 高影响因子
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