Exploring the impact of coffee consumption on liver health: A comprehensive bibliometric analysis.

The study indicates that while research has demonstrated the potential of coffee to mitigate liver damage, a comprehensive quantitative analysis of its effects has yet to be conducted. This study seeks to explore the current landscape and focal points of research on coffee consumption's impact on the liver from 2013 to 2023. Articles published within this timeframe were retrieved from the Web of Science database and subjected to analysis using R software, VOSviewer, and CiteSpace software. A total of 1106 articles primarily focused on coffee's impact on liver health were analyzed. The frequency of publication exhibited a significant increase from 2013 to 2023. The United States emerged as the leading contributor in publications and international collaborations, particularly with institutions such as Harvard Medical School and Harvard T.H. Chan School of Public Health. Noteworthy journals in this domain included "Nutrients" and "Hepatology" Commonly occurring keywords encompassed components, chlorogenic acids, oxidative stress, and liver. The study highlighted coffee's potential benefits in preventing cardiovascular and liver diseases, attributed to mechanisms such as antioxidant activity and modulation of hepatic cells. Through bibliometric analysis, this study offers valuable insights into the research status and emphasis on coffee's effects on liver health, serving as a significant reference for future investigations in this area.

Metabolomics study of the hepatoprotective effect of total flavonoids of Mallotus apelta leaf in carbon tetrachloride-induced liver fibrosis in rats.

Mallotus apelta leaf, recorded in the quality standard of Yao Medicinal Material in Guangxi Zhuang autonomous region, is commonly used in the treatment of liver diseases. Total flavonoids of M. apelta leaf (TFM) had good anti-fibrosis activity, but the anti-fibrosis mechanism of TFM is still unclear. Nuclear magnetic resonance technology was used to study the dynamic changes of urine metabolites in CCl4 -induced liver fibrosis before and after TFM treatment. Ingenuity Path Analysis (IPA) was used to find potential target genes for TFM to improve liver fibrosis and verify the expression of target genes by real-time fluorescent quantitative PCR and Western blotting. TFM can significantly reduce serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) levels, improve liver steatosis and reduce inflammation; in urine metabolomics, a total of seven potential biomarkers were found, mainly involving two metabolic pathways; IPA analysis showed that TNF may be a potential target for TFM to improve liver fibrosis induced by CCl4 in rats. This study found that TNF may be a potential target gene for TFM treatment of liver fibrosis, and shows that the anti-fibrosis mechanism of TFM could improve liver fibrosis by regulating the tricarboxylic acid cycle and subtaurine metabolism.

Efficacy and safety of LY01005 versus goserelin implant in Chinese patients with prostate cancer: A multicenter, randomized, open-label, phase III, non-inferiority trial.

BACKGROUND: LY01005 (Goserelin acetate sustained-release microsphere injection) is a modified gonadotropin-releasing hormone (GnRH) agonist injected monthly. This phase III trial study aimed to evaluated the efficacy and safety of LY01005 in Chinese patients with prostate cancer. METHODS: We conducted a randomized controlled, open-label, non-inferiority trial across 49 sites in China. This study included 290 patients with prostate cancer who received either LY01005 or goserelin implants every 28 days for three injections. The primary efficacy endpoints were the percentage of patients with testosterone suppression ≤50 ng/dL at day 29 and the cumulative probability of testosterone ≤50 ng/dL from day 29 to 85. Non-inferiority was prespecified at a margin of -10%. Secondary endpoints included significant castration (≤20 ng/dL), testosterone surge within 72 h following repeated dosing, and changes in luteinizing hormone, follicle-stimulating hormone, and prostate specific antigen levels. RESULTS: On day 29, in the LY01005 and goserelin implant groups, testosterone concentrations fell below medical-castration levels in 99.3% (142/143) and 100% (140/140) of patients, respectively, with a difference of -0.7% (95% confidence interval [CI], -3.9% to 2.0%) between the two groups. The cumulative probabilities of maintaining castration from days 29 to 85 were 99.3% and 97.8%, respectively, with a between-group difference of 1.5% (95% CI, -1.3% to 4.4%). Both results met the criterion for non-inferiority. Secondary endpoints were similar between groups. Both treatments were well-tolerated. LY01005 was associated with fewer injection-site reactions than the goserelin implant (0% vs . 1.4% [2/145]). CONCLUSION: LY01005 is as effective as goserelin implants in reducing testosterone to castration levels, with a similar safety profile. TRIAL REGISTRATION: ClinicalTrials.gov, NCT04563936.

Integrative Analysis of Transcriptome and Metabolome to Illuminate the Protective Effects of Didymin against Acute Hepatic Injury.

Based on the multiomics analysis, this study is aimed at investigating the underlying mechanism of didymin against acute liver injury (ALI). The mice were administrated with didymin for 2 weeks, followed by injection with lipopolysaccharide (LPS) plus D-galactosamine (D-Gal) to induce ALI. The pathological examination revealed that didymin significantly ameliorated LPS/D-Gal-induced hepatic damage. Also, it markedly reduced proinflammatory cytokines release by inhibiting the TLR4/NF-κB pathway activation, alleviating inflammatory injury. A transcriptome analysis proved 2680 differently expressed genes (DEGs) between the model and didymin groups and suggested that the PI3K/Akt and metabolic pathways might be the most relevant targets. Meanwhile, the metabolome analysis revealed 67 differently expressed metabolites (DEMs) between the didymin and model groups that were mainly clustered into the glycerophospholipid metabolism, which was consistent with the transcriptome study. Importantly, a comprehensive analysis of both the omics indicated a strong correlation between the DEGs and DEMs, and an in-depth study demonstrated that didymin alleviated metabolic disorder and hepatocyte injury likely by inhibiting the glycerophospholipid metabolism pathway through the regulation of PLA2G4B, LPCAT3, and CEPT1 expression. In conclusion, this study demonstrates that didymin can ameliorate LPS/D-Gal-induced ALI by inhibiting the glycerophospholipid metabolism and PI3K/Akt and TLR4/NF-κB pathways.

Bibliometric and visual analysis in the field of tea in cancer from 2013 to 2023.

Objective: Tea has been utilized in cancer research and is progressively gaining wider recognition, with its roles in cancer prevention and treatment being increasingly affirmed. The objective of this study is to investigate the current state and research hotspots in the field of tea's involvement in cancer research from 2013 to 2023, aiming to offer reference and direction for future studies. Methods: We analyzed 4,789 articles published between 2013 and 2022 from the Web of Science database using VOSviewer, R software, and CiteSpace software. Result: Tea-related cancer research showed an overall upward trend, with China leading in publications, followed by the United States, India, Japan, and Italy. China also had significant international collaborations, notably with Harvard University and the Egyptian Knowledge Bank. The 'Journal of Agricultural and Food Chemistry' was the most cited journal. Key topics included 'green tea,' 'cancer,' 'in vitro,' 'oxidative stress,' and 'apoptosis.' Research focused on tea's pharmacological effects, anticancer properties, mechanisms of natural compounds (e.g., polyphenols and EGCG), antioxidant and antimicrobial properties, and molecular mechanisms in cancer treatment. Conclusion: Tea's potential as an anti-cancer medication is gaining global recognition. Our study provides a comprehensive analysis of tea-related cancer research from 2013 to 2023, guiding future investigations in this field.

Isovitexin protects against acute liver injury by targeting PTEN, PI3K and BiP via modification of m6A.

Isovitexin (IVT) has been shown to have a potential therapeutic effect on acute liver injury (ALI), but its underlying mechanisms especially the targets remain unclear, which was investigated in the present study. Briefly, the targets of IVT were predicted by bioinformatics and then were verified by multiple examinations using molecular docking, cellular thermal shift assay (CETSA), and Lipopolysaccharide/D-Galactosamine (LPS/D-GalN)-induced ALI animal model. The bioinformatic analysis predicted that the target genes of IVT against ALI were enriched into the PI3K/Akt and ERS-related pathways, in which, molecular docking and CETSA examination verified that the binding sites of IVT likely were PTEN, PI3K and BiP. Furthermore, the possible targets were also verified by animal experiments. The results revealed that IVT significantly ameliorated the hepatic injury, as evidenced by the attenuation of histopathological changes and the reduction in serum aminotransferase and total bilirubin activities. In addition, IVT treatment led to the reduction of PTEN, BiP and ERS-related targets expressions, as well as the elevation of PI3K, Akt and mTOR expressions. Notably, IVT significantly decreased total hepatic m6A level and m6A enrichment of PTEN and BiP, suggesting IVT regulated PTEN and BiP by modulating m6A modification. To sum up, the results indicate that IVT significantly ameliorates ALI, which is attributed to its ability to regulate the PI3K/Akt pathway and ERS by targeting PTEN, PI3K and BiP via modification of m6A. Our finding demonstrates that IVT may be a promising natural medicine for the treatment of ALI.

Didymin ameliorates dexamethasone-induced non-alcoholic fatty liver disease by inhibiting TLR4/NF-κB and PI3K/Akt pathways in C57BL/6J mice.

The present study aimed to investigate the protective effects and mechanisms of Didymin from Mentha spicata on non-alcoholic fatty liver disease (NAFLD) induced by dexamethasone and high-fat diet (DEX/HFD) in C57BL/6J mice. Briefly, mice were acclimated for 5 days and then subjected to DEX/HFD from days 5 to 28; meanwhile, the animals were treated with Didymin or Silibinin from days 12 to 28. Key indicators of NAFLD were then detected, including the pathological changes of liver tissues, serum biochemical indicators, inflammation, oxidative stress, apoptosis and lipid metabolism. Besides, the expressions of pivotal genes and proteins of the TLR4/NF-κB and PI3K/Akt pathways were examined to further elucidate the mechanisms of Didymin. The results demonstrated that Didymin significantly extenuated hepatocyte damage and lipid disorder. Moreover, Didymin markedly decreased hepatocyte apoptosis by regulating the expressions of B-cell lymphoma-2 (Bcl-2) family and the expressions of the caspase family. Further study elucidated that Didymin decreased the expressions of toll-like receptor 4 (TLR4), as well as the phosphorylation of inhibitor of nuclear factor kappa-B (IκB) and nuclear factor kappa-B p65 (NF-κB p65), suggesting the inhibition of Didymin on the TLR4/NF-κB pathway. Similarly, the PI3K/Akt pathway was also inhibited by Didymin, as evidenced by the decrease in the phosphorylation levels of PI3K and Akt. In summary, this study indicates that Didymin mitigates NAFLD by alleviating lipidosis and suppressing the TLR4/NF-κB and PI3K/Akt pathways, which may be a potential natural medicine for the treatment of NAFLD.

Asiatic acid ameliorates acute hepatic injury by reducing endoplasmic reticulum stress and triggering hepatocyte autophagy.

Endoplasmic reticulum stress (ERS), mutual crosstalk between autophagy and apoptosis-related signaling pathway, plays an important role in the process of acute liver injury (ALI). The present study was to investigate the effects and underlying mechanisms of Asiatic acid from Potentilla chinensis (AAPC) on ALI. The model of ALI in mice was induced by administration with Lipopolysaccharide/D-Galactosamine (LPS/D-GalN). The effects of AAPC on hepatic pathology and hepatocyte apoptosis were observed by hematoxylin-eosin (H&E) staining and TUNEL staining. Serum transaminases activities were measured using an automated biochemical analyzer. Moreover, ERS and autophagy were induced in LO2 cells, respectively. Cell cycle and apoptosis were analyzed using flow cytometry. In addition, ERS and autophagy-related pathways were detected in vivo and in vitro. The results showed that AAPC significantly ameliorated LPS/D-GalN-induced ALI in mice, as evidenced by the improvement of liver pathology and the decrease in serum alanine aminotransferase (ALT) and aspartate transaminase (AST) activities. Moreover, AAPC pre-treatment markedly inhibited thapsigargin-induced cell apoptosis, accompanied by cell cycle arrest at S/G1 phase in LO2 cells. AAPC notably inhibited the activation of the PERK/ATF6 and IRE1 pathway, alleviating the extent of ERS. Additionally, AAPC significantly promoted autophagy, as evidenced by the increase in the formation of autophagic vacuoles and the number of autophagosomes as well as the increased expressions of LC3II/I, Beclin-1, Atg5 and Atg7. In summary, our results indicate that AAPC significantly ameliorates ALI by inhibiting the ERS pathway and promoting hepatocyte autophagy.

Asiatic acid from Potentilla chinensis alleviates non-alcoholic fatty liver by regulating endoplasmic reticulum stress and lipid metabolism.

Endoplasmic reticulum stress (ERS) is induced by accumulation of misfolded proteins, playing a pivotal role during the processes of non-alcoholic fatty liver disease (NAFLD). The present study was to investigate the effect of Asiatic acid from Potentilla chinensis (AAPC) on liver cell lipid metabolism, exploring the underlying mechanism of AAPC against NAFLD. In vivo, the animal NAFLD model was induced by feeding rats with high fat diet (HFD) for 18 weeks, and meanwhile the rats were treated with AAPC from weeks 8 to 18; In vitro experiment, the effect of AAPC on dyslipidemia induced by oleic acid (OA) in hepatic cells (HepG2) was evaluated. The results showed that AAPC significantly decreased lipidosis in rats and in HepG2 cells; it notably alleviated hepatocyte damage and lipid disturbance in rats. Moreover, the cell experiments showed that AAPC strongly inhibited HepG2 cell proliferation. It markedly decreased hepatocyte lipogenesis by regulating the key lipid metabolism-related factors, such as sterol regulatory element-binding protein 1c (SREBP-1c), encoding carboxylase, liver X Receptor Rα (LXRα), fatty acid synthase (FAS), and AMP-activated protein kinase (AMPK). The further study elucidated that AAPC treatment significantly alleviated inflammatory response by inhibiting the nuclear factor-kappa B (NF-kB) pathway. Moreover, AAPC significantly alleviated hepatocyte apoptosis and lipid metabolism disorder through reducing the extent of ERS. In conclusion, our study demonstrates that AAPC significantly ameliorates NAFLD by inhibiting the ERS pathway and lipid deposition, which may be a potential natural medicine for the treatment of NAFLD.

Effect of passive pile on 3D ground deformation and on active pile response.

Using a series of model tests, this study investigated the effect of a passive pile on 3D ground deformation around a laterally loaded pile and on that laterally loaded pile's response in sand. The active pile head was subjected to lateral loads, and the passive pile was arranged in front of the active pile. In the model tests, the distance between the two pile centers was set to zero (i.e., a single pile test), 2.5, 4, and 6 times the pile width (B). The 3D ground surface deformations around the active and passive piles were obtained using a newly developed Stereo-PIV technique. The experimental results showed that the ground surface movements were restrained by the passive pile when the pile spacing was less than 6B. The response of the active pile was affected by the passive pile when the pile spacing was less than 4B. This study combined the response of the active pile and surrounding 3D ground deformation to investigate the effect of the passive pile, which is useful to further understand the pile-soil-pile interactions and to enhance pile foundation design in engineering practice.