文献检索

查找使用阿拉丁产品的科研文献

检索与阿拉丁产品相关的同行评审论文、DOI、PubMed 编号、期刊、作者、CAS 号及研究领域。

科研影响力快照

与阿拉丁产品相关的已发表科研成果

在搜索之前,这些指标可帮助访客快速了解产品关联科研的规模与质量。

346,364+ SCI 论文 与阿拉丁产品引用相关
2,295,288.15 总影响因子 匹配文献记录中影响因子的总和
81.20 最高期刊影响因子 匹配期刊中的最高 IF
6.63 平均期刊影响因子 匹配文献的平均 IF

参考指标 指标基于阿拉丁文献引用数据库及期刊影响因子记录。文献关联仅供科研参考,请以原始文献为准。

热门产品

视图 列表 网格

显示第1至12个,产品总数59个

设置提升方向
CCL4
Nanoscale · 2025 · IF 5.1

Synthesis of MXene/carbon composites via controlled etching of Ti3SiC2 in the gaseous etchant CCl4

Yu Wang,Xudong Wang,Mian Li,Zhifang Chai,Qing Huang

The study investigates the structural evolution of Ti3SiC2 using the gaseous etchant CCl4, emphasizing its ability to selectively etch Si and Ti atoms to form an MXene (Ti3C2Cl2)/carbon composite and carbide-derived carbon (CDC). Under specific conditions, a complete conversion to the MXene is accomplished at a Ti3SiC2 : CCl4 molar ratio of 1 : 3.5, whereas higher CCl4 concentrations lead to further oxidation of Ti3C2Cl2 and formation of lamella CDC. This method presents an alternative chemical etching route to synthesize MXenes. Importantly, the production of CDC using CCl4 as an etchant could obtain carbon/MXene hybrids with significant implications for promising energy storage applications.

CAS / MDL: 10108-64-2
研究领域: 材料科学 · 能源存储
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
JOURNAL OF ETHNOPHARMACOLOGY · 2017 · IF 2.981

Hepatoprotective activities of Antrodia camphorata and its triterpenoid compounds against CCl4-induced liver injury in mice

Zi-wei Li,Yi Kuang,Shu-nan Tang,Kai Li,Yun Huang,Xue Qiao,Si-wang Yu,Yew-min Tzeng,Jen-Yu Lo,Min Ye

Ethnopharmacology relevance Antrodia camphorata (AC) is a rare and precious fungus indigenous to Taiwan used as a traditional medicine for the treatment of liver injury. Triterpenoids are the major bioactive constituents of A. camphorata and have been reported to possess hepatoprotective activities. To meet the increasing demand, artificial cultivation techniques have been developed. Aim of the study This study aims to evaluate the hepatoprotective activities of AC samples derived from different cultivation techniques and to dissect the main active triterpenoid compounds. Materials and methods The ethanol extracts of five batches of AC samples, including wild growing fruiting bodies, cutting wood culture fruiting bodies, dish cultures, cutting wood culture mycelia, and submerged fermentation mycelia were orally administered (50   mg/kg or 200   mg/kg) to ICR mice for 7 days. On the last day, CCl 4 (0.2%, 7   mL/kg, i.p.) was used to induce liver injury, and the activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined 24   h after the injection. Moreover, a HepG2 cell model treated with CCl 4 (0.35%) was used to screen the protective activities of 29 AC triterpenoids. After incubation for 6   h, viabilities of the cells were tested using MTS assay. The in vivo hepatoprotective activities of antcin B and antcin K were further studied on the mice model by ALT and AST tests and histopathologic examinations. To elucidate the mechanisms, the mRNA levels of iNOS , COX2, TNF-α and IL-1β, and the protein levels of NF-κB (p65/p-p65), iNOS and COX2 in liver tissues were determined. Results The wild growing or cutting wood culture fruiting bodies, and the dish cultures of AC showed more potent activities than the mycelia ( P <0.001). At 20   μM, 16 of 29 triterpenoids showed significant protective activities, increasing HepG2 cell viability from 46% of the CCl 4 group to >90%. Antcin B and antcin K could dose-dependently (10 or 50   mg/kg, 7 days, i.g.) decrease the serum levels of ALT and AST, and decrease the incidence of liver necrosis . The effects of 50   mg/kg of antcin K or antcin B were almost identical to those of 100   mg/kg silymarin . Furthermore, qRT-PCR and Western blotting analyses revealed they could down-regulate IL-1β, TNF-α, iNOS, COX-2 and NF- κ B in liver tissues at both transcriptional and translational levels. Conclusion The results indicate that cultivation techniques remarkably affect the hepatoprotective activities of AC. Antcin K and antcin B are the major hepatoprotective compounds of A. camphorata , and the mechanism is related with anti-inflammation. Given its high natural abundance and good oral absorption, antcin K could be a promising drug candidate for liver injury.

CAS / MDL: 56-23-5
研究领域: 药理学 · 中药学 · 肝脏病学
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
Food & Function · 2020 ·Vol. 11 ·期 6 ·5156-5165 · IF 4.171

Pelargonidin ameliorates CCl4-induced liver fibrosis by suppressing the ROS-NLRP3-IL-1β axis via activating the Nrf2 pathway

Yu-Sheng Shi,Xiao-Xing Li,Hao-Tian Li,Yan Zhang

Liver fibrosis is a histological change that often occurs due to hepatic stellate cell (HSC) activation and excessive formation of an extracellular matrix in the liver. Pelargonidin (PEL) is a natural anthocyanidin existing in blueberries, berries, strawberries, and red radishes and has been demonstrated to possess health beneficial effects. Herein, we investigated the effect of PEL on liver fibrosis induced by CCl4 and hepatic stellate cells induced by transforming growth factor-β (TGF-β). We found that PEL administration prevented liver injury and liver fibrosis induced by CCl4 in a dose-dependent manner. Further data revealed that PEL increased liver nuclear factor E2-related factor 2 (Nrf2) and reduced liver oxidative stress and the expression levels of NLRP3, caspase-1 and IL-1β. In TGF-β-challenged HSCs (LX-2 cells), PEL effectively inhibited the LX-2 cell activation. In addition, the anti-fibrosis effects of PEL in LX-2 cells were abolished by Nrf2 knockdown. In summary, our study demonstrated that PEL ameliorated CCl4-induced liver fibrosis and HSC activation induced by TGF-β. The possible molecular mechanisms of PEL in liver fibrosis may be attributed to its suppression of ROS-NLRP3-IL-1β signaling by Nrf2 activation.

CAS / MDL: 56-23-5 134-04-3
研究领域: 药理学 · 肝病学 · 分子生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
TALANTA · 2020 · IF 5.339

Novel near-infrared fluorescence probe with large Stokes shift for monitoring CCl4-induced toxic hepatitis

Yang Tian,Dong-Ye Zhou,Wen-Li Jiang,Zun-Pan She,Yongfei Li,Chun-Yan Li

Toxic hepatitis which is induced by chemical substance is a serious threat to human health. More and more studies have shown that peroxynitrite (ONOO − ) is related with the development of toxic hepatitis. So it is important to find a tool to study ONOO − change during the diagnosis and therapy of toxic hepatitis. Herein, a series of novel near-infrared (NIR) fluorescence dyes (DDM-R) with long emission wavelength (740–770 nm) and large Stokes shift (~200 nm) are developed. Among the dyes, DDM-OH with great spectral performance and facilely modified feature is used to construct probe DDM-ONOO - . The probe have the preference of high sensitivity and excellent selectivity for ONOO − . In addition, DDM-ONOO - was applied in detecting exogenous and endogenous ONOO − in cells and further used in detecting ONOO − of CCl 4 -induced toxic hepatitis in cells by fluorescence imaging, 3D quantification analysis, flow cytometry . More importantly, by visualizing ONOO − , the probe was used to monitor the diagnosis of CCl 4 -induced toxic hepatitis in mice and evaluate the therapeutic efficacy of hepatoprotective medicines (NAC, SM, DDB). The results show that the probe will provide a powerful tool for the diagnosis and treatment of toxic hepatitis.

研究领域: 化学 · 药理学 · 医学诊断
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
JOURNAL OF NUTRITIONAL BIOCHEMISTRY · 2024 · IF 4.8

Lipidomic profiling of serum and liver tissue reveals hepatoprotective mechanism of taxifolin in rats with CCl4-induced subacute hepatic injury based on LC-MS/MS

Yiming Ni,Xinghua Chen,Yiqun Jia,Long Chen,Mingmei Zhou

Currently, the hepatoprotective activity of taxifolin, a flavonoid isolated from Pseudotsuga taxifolia , has been reported in many animal models. However, whether the protective effect of taxifolin on the liver is related to its effect on lipidomics is unclear. Based on the significant therapeutic effect of taxifolin on CCl 4 induced subacute hepatic injury, we observed the intervention of taxifolin by lipidomics. The results demonstrate that taxifolin can effectively reverse the damage caused by CCl 4 , which including hepatocyte vacuolization and necrosis. Lipomic profiling based on liquid chromatography-mass spectrometry showed that taxifolin was able to restore lipidomic changes caused by CCl 4 , including the levels of lysophosphatidylserine (LPS), phosphatidylcholine (PC), coenzyme (Co), phosphatidylglyceride (PG), phosphatidylserine (PS), dimethylphosphatidylethanolamine (dMePE), ceramide (Cer), sphingosine (So), triglycerides (TG), and monogalactosyl diacylglycerol (MGDG) in the rat liver, and phosphatidylcarbinol (PMe) and phosphatidylethanolamine (PE), plant sphingosine (phSM), glucose ceramide (CerG1), TG, and diglycerides (DG) in serum. Spearman's correlation analysis showed that CerG1, phSM, PE, and PMe in serum, and Cer, dMePE, PG, PS, So, TG, and MGDG in liver were positively correlated with serum levels of aspartate transaminase, alanine transaminase, and liver index; while TG, DG in serum, and Co, LPS, PC in liver were negatively correlated with the parameters. In total, 43 and 34 lipid molecules were altered by taxifolin treatment in the liver and serum, respectively, mainly including glycerophosphoglycerols, glycerophosphocholines, glycerophosphoethanolamines, and linoleic acids and derivatives. Our findings help to provide novel insights into the mechanism of the hepatoprotective effect of taxifolin from a lipidomics approach.

CAS / MDL: 56-23-5
研究领域: 药理学 · 代谢组学 · 肝脏病学
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
Food Science & Nutrition · 2023 · IF 3.9

Mulberroside A ameliorates CCl4-induced liver fibrosis in mice via inhibiting pro-inflammatory response

Baozhang Shi,Jinqiang Qian,Hongyue Miao,Shuo Zhang,Yue Hu,Puqing Liu,Liping Xu

Liver fibrosis is caused by a variety of pathogenic factors. It is mainly characterized by chronic liver damage mediated by the imbalance between extracellular matrix synthesis and degradation. If the injury factor cannot be removed for a long time, fibrosis will progress to cirrhosis or even cancer. The development of liver fibrosis is a very complex process which is related to the activation of hepatic stellate cells (HSCs), oxidative stress, and cytokines produced by immune cells. At present, screening of substances with anti-inflammatory activity from natural plant extracts has become a new research focus in the prevention and treatment of liver fibrosis. Mulberry twig is a commonly used traditional Chinese medicine. Pharmacological studies have shown that mulberry twig has anti-inflammatory and antioxidant activities. Thus, it is likely that Mulberry twig contains active substances with liver protection functions. The present study aimed to explore the effect of Mulberroside A (MulA), the main active ingredient from Mulberry twig, on acute liver injury induced by CCl 4 in mice. MulA treatment could significantly alleviate the CCl 4 -induced liver injury, as evidenced by histological analysis and Masson staining. However, we observed that MulA inhibited the expressions of collagen I and α-SMA in livers of CCl 4 -treated mice but did not directly inhibit the proliferation and activation of HSCs. Finally, we analyzed the anti-inflammatory effect of MulA and demonstrated that it could markedly inhibit the pro-inflammatory cytokines release in liver tissues and in cultured macrophages, thereby alleviating liver fibrosis. Our findings suggest MulA as a potential therapeutic candidate for liver injury and inflammatory diseases.

CAS / MDL: 56-23-5
研究领域: 药理学 · 肝病学 · 免疫学 · 分子生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
TOXICOLOGY AND APPLIED PHARMACOLOGY · 2023 · IF 3.8

Dihydrokaempferol attenuates CCl4-induced hepatic fibrosis by inhibiting PARP-1 to affect multiple downstream pathways and cytokines

Hancheng Huang,Shuchun Wei,Xiaohan Wu,Mengke Zhang,Benhong Zhou,Debin Huang,Weiguo Dong

The pathophysiological mechanism of hepatic fibrosis (HF) is related to the excessive activation of the DNA repair enzyme poly ADP-ribose polymerase-1 (PARP-1). The drugs, targeting PARP-1, are scarce. Therefore, the lead compound, moderately inhibiting PARP-1, with anti-HF properties should be identified. This study screened dihydrokaempferol (DHK) from herbs based on preliminary studies to intervene in a CCl 4 -induced liver injury and HF model in mice. In vitro , the expression levels of PARP-1-regulated related proteins and phosphorylation were examined. The binding pattern of DHK and PARP-1 was analyzed using molecular docking and molecular dynamics platforms. The results showed that DHK could significantly attenuate CCl 4 -induced liver injury and HF in mice. Moreover, it could also attenuate the toxic effects of CCl 4 on HepG2 and inhibit α-SMA and Collagen 1/3 synthesis of LX-2 cells in-vitro . Molecular docking revealed that DHK could competitively bind to the Glu-988 and His-862 residues of the upstream DNA repair enzyme PARP-1, moderately inhibiting its overactivation. This led to maintaining NAD + levels and energy metabolism in hepatocytes and inhibiting the activation of PARP-1-regulated downstream signaling pathways (TGF-β1, etc. ), related proteins (p-Smd2/3, etc. ), and inflammatory mediators while acting indirectly. Thus, DHK could attenuate CCl 4 -induced liver injury and HF in mice in a different mechanism from those of the existing reported flavonoids. It was associated with inhibiting the expression of downstream pathways and related cytokines by competitively binding to PARP-1. This study might provide a basis and direction for the design and exploration of anti-HF lead compounds.

CAS / MDL: 56-23-5 8001-25-0
研究领域: 药理学 · 肝病学 · 分子生物学 · 毒理学
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
Journal of Functional Foods · 2025 · IF 4

Elucidation of the mechanism of the fruit of Rubus chingii Hu against CCl4-induced liver injury in mice based on met/Tlr2/Tlr4 -mediated PI3K-Akt signaling pathway

Ping Jiang,Yanfei He,Guangpei Xu,Chuanbo Sun

This study aims to evaluate the mechanism of RCH against CCl 4 -induced liver injury in mice. RCH treatment effectively inhibited CCl 4 -induced liver injury and apoptosis in mice, and reduced liver enzyme activities, blood inflammatory cell and serum inflammatory factor levels. Network pharmacology and machine learning predicted that PI3K-Akt pathway and Met proteins play important roles in RCH anti-CCl 4 -induced liver injury. The results of qRT-PCR and Western blot showed that RCH could down-regulate the expression of the receptor proteins Met, Tlr2, and Tlr4, and inhibit the phosphorylation of Pik3ca and Akt1, and prevent the phosphorylation of NF-κB P65, and decrease cleaved Caspase3 expression. These findings suggest that RCH effectively alleviated liver injury in CCl 4 -induced mice by inhibiting the Met/Tlr2/Tlr4-mediated PI3K-Akt signaling pathway.

研究领域: 药理学 · 分子生物学
✓ 已验证 DOI 高影响因子
查看原文 查看 PubMed
JOURNAL OF NANOBIOTECHNOLOGY · 2025 ·Vol. 23 ·期 1 ·1-26 · IF 12.6

Co-encapsulation of norcantharidin prodrugs and lomitapide in nanoparticles to regulate CCL4 expression by inhibiting Wnt/β-catenin pathway for improved anti-tumor immunotherapy

Zhao Feng,Gong Liming,Wang Ping,Chen Dong,Cao Shijie,Yang Feifei,Tang Manqing,Meng Yuanyuan,Wang Yuming,Miao Lin,Li Yunfei,Huang Wei

In the absence of tumor antigen specificity, direct chemokine administration carries the risk of significant “on-target, off-tumor” toxicities, highlighting the need for small-molecule approaches with reduced immunogenicity. This study investigates the synergistic potential of norcantharidin (NCTD) and lomitapide (lomi) in selectively restoring CCL4 expression by deactivating the tumor intrinsic β-catenin pathway. Due to its similar lipophilicity to lomi and potential to suppress β-catenin, NCTD prodrug (C12) was selected to be co-encapsulated with lomi in a nanoparticle-mediated co-delivery system (NP“C12 + lomi”). The NP“C12 + lomi” formulation exhibited a high encapsulation rate, uniform particle size, and suitability for therapeutic use. It effectively inhibited the proliferation of 4T1 cells and restored CCL4 expression. In both primary breast tumor and surgically resected tumor mouse models, NP“C12 + lomi” significantly increased the proportion of CD8 + cells in primary tumors, blood, and lung metastases, approximately doubling their presence. This led to a prolongation of median survival in mice to 59 days. Furthermore, when combined with an immune checkpoint inhibitor, NP“C12 + lomi” substantially inhibited tumor growth and lung metastasis without affecting body weight or causing major tissue or organ damage. This was attributed to the controlled dissociation of the nanoparticle and the subsequent modulation of C12 and lomi, which mitigated CCL4-related toxicity. This study provides valuable insights into the safe production of chemokines using a small-molecule pair through a nanosystem and presents a robust chemo-immunological cascade therapy strategy, demonstrating significant efficacy against malignant metastatic tumors. Graphical abstract

研究领域: 肿瘤学 · 免疫学 · 药剂学 · 分子生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
CHEMICO-BIOLOGICAL INTERACTIONS · 2025 · IF 5.4

Hypoxia-inducible factor-1 alpha (HIF-1α) inhibitor AMSP-30 m attenuates CCl4-induced liver fibrosis in mice by inhibiting the sonic hedgehog pathway

Lili Lu,Yuchen Ma,Qing Tao,Jing Xie,Xiao Liu,Yongkang Wu,Yang Zhang,Xiuli Xie,Mingming Liu,Yong Jin

Liver fibrosis is a passive and irreversible wound healing process caused by chronic liver injury. Research has shown that the upregulation of hypoxia inducible factor-1 alpha (HIF-1α) is closely related to the occurrence and development of liver fibrosis and HIF-1 α may be a promising target for the treatment of liver fibrosis. AMSP-30 m is a newly developed novel HIF-1α inhibitor by our group, which has strong anti-tumor and anti-inflammatory effects. In this study, we described the therapeutic effect and specific mechanism of AMSP-30 m on carbon tetrachloride (CCl 4 ) induced liver fibrosis in mice. Liver fibrosis induced by CCl 4 in mice and liver fibrosis induced by cobalt dichloride (CoCl 2 ) in LX-2 cells (human hepatic stellate cell (HSC) line) were studied. Hematoxylin & eosin (H&E)and Masson's trichrome staining were used to observe pathological conditions. Western Blot, immunofluorescence and immunohistochemistry were used to detect protein expression and localization in cells, and quantitative real-time PCR analysis (qRT-PCR) was used to detect mRNA expression. Biochemical detection kits were used to detect alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. The results demonstrated that AMSP-30 m significantly alleviated pathological symptoms, reduced ALT and AST levels, and inhibited the expression of alpha-smooth muscle actin (α-SMA) and collagen type I (COL1α1) in CCl 4 -induced liver fibrosis in mice. AMSP-30 m could significantly reduce the expression of HIF-1α and sonic hedgehog (Shh) pathway related proteins (Smoothened (Smo), Shh, and glioma-associated oncogene-1 (Gli-1)) in CCl 4 induced liver fibrosis mice. AMSP-30 m also played a similar role in the CoCl 2 -induced anoxic liver fibrosis model of LX-2 cells . Further experiments showed that Cyclopamine (a Shh inhibitor) could significantly inhibit the increase of α-SMA and COL1α1 resulting from HIF-1α but not significantly inhibit HIF-1α induced by CoCl 2 in LX-2 cells. And the combination of Cyclopamine and AMSP-30 m further reduced the expression of α-SMA and COL1α1 induced by HIF-1α. In summary, this study demonstrates that the HIF-1α inhibitor AMSP-30 m exerts a robust anti-fibrotic effect by inhibiting the Shh pathway, which is identified as a critical underlying mechanism. These findings suggest a promising therapeutic strategy for the treatment of liver fibrosis.

研究领域: 分子生物学 · 药理学 · 肝病学 · 细胞生物学 · 生物化学
✓ 已验证 DOI PubMed 高影响因子
查看原文 查看 PubMed
INTERNATIONAL IMMUNOPHARMACOLOGY · 2023 · IF 5.6

Sodium alginate combined with oxymatrine ameliorates CCl4-induced chemical hepatic fibrosis in mice

Chen He,Wenjing Wang,Guoli Wei,Yuqing Wang,Yingjie Wei,Jing Wang,Zhenhai Zhang

Hepatic fibrosis (HF) is a challenging clinical problem. Both sodium alginate (SA) and oxymatrine (OM) can be used to treat HF; however, the influence of viscosity on the therapeutic efficacy of sodium alginate is currently unknown. This study used a CCl 4 -induced HF mouse model to screen the specifications and doses of SA and investigate its therapeutic effects on HF in combination with OM. Sodium alginate of different viscosities ameliorated HF in mice, with 232 mPa·s SA delivered at a dose of 100 mg/kg showing remarkable therapeutic effect, characterized by reduced aspartate transaminase/alanine transaminase levels, reduced expression of α-SMA, collagen I, and other related genes, and increased abundance of beneficial intestinal probiotics such as Lactococcus and Blautia . The combination treatment further improved other related indices and increased the abundance of Phascolarctobacterium and Oscillospiraceae. These results suggest that the oral administration of SA may improve HF via the “gut-liver axis” based on the gut microbiota and has potential clinical applications.

CAS / MDL: 16837-52-8
研究领域: 药理学 · 肝病学 · 微生物学 · 病理学
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
ACTA BIOCHIMICA POLONICA · 2022 ·Vol. 69 ·期 2 ·363-370 · IF 2.349

6-Shogaol alleviates CCl4-induced liver fibrosis by attenuating inflammatory response in mice through the NF-κB pathway

Jian-li Qiu,Yu-na Chai,Feng-yang Duan,Hui-juan Zhang,Xiao-yan Han,Ling-yan Chen,Fei Duan

Liver fibrosis is a global health problem caused by a number of diseases related to liver damage. 6-Shogaol is a biologically active substance derived from the rhizome of Zingiber officinale Roscoe with anti-tumor, anti-inflammatory, and antioxidant properties. To explore the effects of 6-Shogaol on liver fibrosis, we used a mouse model of the condition in which mice were injected intraperitoneally with carbon tetrachloride (CCl4) at a dose of 2 mL/kg three times per week for a period of 4 weeks. 6-Shogaol was administered orally at two different doses (5 mg/kg, 20 mg/kg) 30 min before CCl4 injection. CCl4 induced severe liver injury and fibrosis, as indicated by significant inflammatory cell infiltration, disordered liver structure, increased activities of aspartate aminotransferase and alanine aminotransferase (liver damage markers) in serum, elevated collagen deposition, and overexpressed alpha-smooth muscle actin (α-SMA, marker of hepatic stellate cells activation) in liver tissues, whereas 6-Shogaol administration rescued those alterations dose-dependently. We found that 6-Shogaol suppressed CCl4-induced inflammatory response by inhibiting macrophage recruitment, release of pro-inflammatory factors, and activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in liver tissues. Additionally, we demonstrated that 6-Shogaol blocked CCl4-induced activation of the nuclear factor-kappa B (NF-κB) pathway, which is a vital transcriptional regulator of the inflammatory response. Altogether, this study demonstrates that 6-Shogaol can prevent CCl4-induced liver fibrosis by suppressing inflammatory response through the NF-κB pathway and suggests that 6-Shogaol can be used for liver fibrosis prevention.

CAS / MDL: 47165-04-8
研究领域: 药理学 · 肝病学 · 免疫学
✓ 已验证 产品关联 DOI PubMed 高影响因子
查看原文 查看 PubMed
已复制

文献关联基于可获得的产品、CAS、DOI 及引用记录。收录不代表作者或出版方对阿拉丁产品的背书,请以原始文献为准。