ETHNOPHARMACOLOGICAL RELEVANCE:Danggui-Shaoyao-San (DGSY) is a classic prescription in traditional Chinese medicine that has demonstrated therapeutic efficacy in treating fatty liver. However, its pharmacological mechanisms remain inadequately explored. AIM OF THE STUDY:This study aims to elucidate the molecular mechanisms through which DGSY may contribute to the modulation of MASH progression. MATERIALS AND METHODS:A MASH model was established in mice using a high-fat high-carbohydrate (HFHC) diet, followed by treatment with DGSY to assess its efficacy. RNA sequencing (RNA-Seq) analysis, western blotting, and immunofluorescence were employed to elucidate the potential mechanisms of DGSY in the treatment of MASH. The MASH mouse model and bone marrow-derived macrophages (BMDMs) stimulated with LPS + ATP were utilized to investigate the activation of the NLRP3 inflammasome in macrophages. Additionally, the mechanisms of DGSY were further validated through NLRP3 knockdown in vivo and knockout in vitro. UHPLC-Q-Orbitrap HRMS analysis was employed to identify the primary active components of DGSY. RESULTS:DGSY was effective in treating the HFHC diet-induced MASH mouse model, significantly alleviating liver inflammation. Mechanistically, RNA-Seq analysis indicated that the NOD-like receptor signaling pathway was significantly affected in DGSY-mediated effects. The protein expression levels of NLRP3, caspase1, and IL-1β were significantly elevated in liver macrophages from the MASH mouse model and in LPS + ATP-stimulated BMDMs, which were reversed by DGSY treatment. NLRP3 knockdown in vivo alleviated MASH but counteracted the therapeutic effects of DGSY. Both NLRP3 knockdown in vivo and knockout in vitro abolished its effect on inhibiting caspase1 activity and IL-1β release. In addition, UHPLC-Q-Orbitrap HRMS analysis identified four main active ingredients in DGSY, with atractenolide III and gallic acid notably inhibiting NLRP3 protein expression. CONCLUSIONS:DGSY exerts a protective effect against MASH, inhibiting hepatic macrophage NLRP3 inflammasome, suppressing caspase1 activity, and reducing IL-1β release. This study provides experimental evidence for the clinical application of DGSY in the treatment of MASH.

Caffeine (CAFF) is abundant in black coffee. As one of the most widely consumed beverages globally, coffee has been the focus of increasing clinical and basic research, particularly regarding its benefits in alleviating metabolic dysfunction-associated steatotic liver disease (MASLD). However, the therapeutic effects of CAFF on metabolic-associated steatohepatitis (MASH) and the underlying mechanisms remain unclear. In this study, we demonstrated that CAFF potently reduced hepatic steatosis, inflammation, and early-stage liver fibrosis in MASH mice induced by prolonged (36 weeks) high-fat high-carbohydrate (HFHC) diets and high-fat diets combined with carbon tetrachloride (CCl4) injections. By using multiple target-identifying strategies, including surface plasmon resonance (SPR), cellular thermal shift assay (CETSA), and drug affinity responsive target stability (DARTS) assay, we identified dual-specificity phosphatase 9 (Dusp9) as a key therapeutic target, which was diminished by HFHC but restored with CAFF treatment. Dusp9 knockdown in vivo and in vitro exacerbated glycolipid metabolism disorders and stunningly counteracted the systemic therapeutic effects of CAFF in the MASH models. In addition, CAFF inactivated the ASK1-p38/JNK, a downstream signaling pathway of Dusp9, which regulates inflammation and apoptosis. Our study highlights the multifaceted benefits of CAFF in treating MASH by rescuing hepatic Dusp9 expression, thereby reversing glycolipid metabolism disorders, liver inflammation, and fibrosis. These findings provide experimental evidence supporting the clinical and daily use of CAFF and black coffee in managing MASH patients.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the predominant chronic liver condition globally. Bile acid (BA) metabolism contributes significantly to MASLD progression. In this multicenter clinical study, we aimed to characterize serum BA profiles in patients with MASLD and identify specific alterations compared to healthy controls. All MASLD cases were sourced from the gastroenterology outpatient departments of Shanghai Baoshan Hospital of Integrated Chinese and Western Medicine, Shanghai Baoshan District Songnan Community Health Service Center, and Lianyungang Oriental Hospital between June 2015 and December 2019. The data were analyzed using SPSS version 26.0, with a p-value of less than 0.05 considered significant. A total of 215 participants (35.3

Polyphenols, known for their potent antioxidant and anti-inflammatory properties, have emerged as promising, natural, and safe complementary treatment options for metabolic-associated steatotic liver disease (MASLD). Among these, curcumin, resveratrol, and silymarin are the most extensively studied; however, their differential effects on MASLD outcomes remain inconclusive. This systematic review and meta-analysis of RCTs aimed to evaluate the efficacy of curcumin, resveratrol, and silymarin in patients with MASLD. A comprehensive search of seven databases was conducted up to September 2024. Odds ratios (OR), mean differences (MD), and standardized MD (SMD) with 95% confidence intervals (CI) were used to assess treatment effects. Primary outcomes included improvement in hepatic steatosis and ALT activity, while secondary outcomes included changes in AST activity, blood lipids, glucose, BMI, blood pressure, and TNF-α. Twenty-seven studies involving 1691 participants were included. Curcumin significantly improved hepatic steatosis compared to placebo (OR: 4.39, 95% CI: 1.45 to 13.27, p = 0.009), followed by resveratrol (OR: 3.18, 95% CI: 1.20 to 8.42, p = 0.02). Silymarin exhibited the strongest effect in reducing ALT levels (MD: -6.44 U/L, 95% CI: -10.03 to -2.85, p = 0.0004), with curcumin (MD: -5.88 U/L, 95% CI: -9.05 to -2.72, p = 0.0003) also showing significant reductions. A marked reduction in AST was observed with silymarin (MD: -6.99 U/L, 95% CI: -8.56 to -5.42, p < 0.00001), followed by curcumin (MD: -3.36 U/L, 95% CI: -5.35 to -1.36, p = 0.001). Furthermore, curcumin intake significantly improved metabolic indicators (TG, FBG, HOMA-IR, and BMI). Resveratrol reduced FBG and DBP. Curcumin had the strongest effect on hepatic steatosis and improved both transaminase levels and metabolic markers. Silymarin demonstrated the greatest reduction in transaminase levels, while resveratrol showed modest benefits in steatosis and metabolic improvements. The three polyphenols appear as promising therapeutics for the treatment of MASLD.

Background Non-alcoholic steatohepatitis (NASH), an escalating global health concern, is a primary factor behind cirrhosis, liver transplantation, and hepatocellular carcinoma. Effective treatments remain elusive. Danggui-Shaoyao-San (DGSY), a classic famous prescription employed in treating NASH, could hold promise, although its molecular underpinnings are still under investigation. This study undertakes an exploration of the impacts of DGSY on NASH and seeks to illuminate the mechanisms at play. Methods UHPLC-Q-Orbitrap HRMS was employed to identify compounds within DGSY. Mice underwent a 25-week regimen of HFHC diet and high-sugar water, with 4 weeks of DGSY treatment for efficacy and pathogenic mechanism exploration in vivo. L02 cells were cultured with 0.2 mM FFA for 24 h, exposed to DGSY at 1 mg/ml and 2 mg/ml for efficacy and pathogenic mechanism exploration in vitro. Using online databases, we sought potential targets for NASH treatment, and through PPI networks, identified key targets. Expression levels of genes and proteins were examined by western blotting, RT-PCR, and immunofluorescence staining. Results Thirty-four compounds were identified within DGSY. DGSY brought about marked reductions in biochemical indicators and yielded significant improvements in NASH mice histological features. Additionally, it mitigated hepatic steatosis and inflammation both in vivo and in vitro. The top 10 targets from two network pharmacology analyses, one focusing on structural prediction and the other on literature mining, identified APOE and APP as potential therapeutic targets for DGSY in NASH treatment. PCR validation confirmed that DGSY reduced APP expression after treatment, and further investigation revealed that DGSY significantly suppressed hepatic APP and Aβ expression, indicating its effectiveness in treating NASH. Furthermore, it inhibited Aβ-induced Cathepsin B lysosomal release, reducing hepatic inflammation. Conclusion Danggui-Shaoyao-San has anti-steatohepatitis effects in ameliorating hepatic APP protein expression, reducing hepatic lysosomal CTSB release, and suppressing hepatic NF-κB activation. The study provided a more theoretical basis for the future clinical application of DGSY.

INTRODUCTION: In metabolic dysfunction–associated steatotic liver disease, the diagnostic efficacy of controlled attenuation parameter (CAP) was not very accurate in evaluating liver fat content. The aim of this study was to develop a score, based on CAP and conventional clinical parameters, to improve the diagnostic performance of CAP regarding liver fat content. METHODS: A total of 373 participants from 2 independent Chinese cohorts were included and divided into derivation (n = 191), internal validation (n = 75), and external validation (n = 107) cohorts. Based on the significant difference index between the 2 groups defined by the magnetic resonance imaging–proton density fat fraction (MRI-PDFF) in derivation cohort, the optimal model (CAP-BMI-AST score [CBST]) was screened by the number of parameters and the area under the receiver operating characteristic curve (AUROC). In the internal and external validation cohorts, the AUROC and corresponding 95% confidence intervals (CIs) were used to compare the diagnostic performance of CBST with that of CAP. RESULTS: We constructed the CBST = −14.27962 + 0.05431 × CAP − 0.14266 × body mass index + 0.01715 × aspartate aminotransferase. When MRI-PDFF was ≥20%, ≥10%, and ≥5%, the AUROC for CBST was 0.77 (95% CI 0.70–0.83), 0.89 (95% CI 0.83–0.94), and 0.93 (95% CI 0.88–0.98), which was higher than that for CAP respectively. In the internal validation cohort, the AUROC for CBST was 0.80 (95% CI 0.70–0.90), 0.95 (95% CI 0.91–1.00), and 0.98 (95% CI 0.94–1.00). The optimal thresholds of CBST were −0.5345, −1.7404, and −1.9959 for detecting MRI-PDFF ≥20%, ≥10%, and ≥5%, respectively. DISCUSSION: The CBST score can accurately evaluate liver steatosis and is superior to the CAP.

Background: PRM1201 is a traditional medicine with beneficial effects against colorectal cancer (CRC) metastasis. However, the underlying mechanism of this action remains to be determined. Hypothesis: Remodeling microbiota and short-chain fatty acids (SCFAs) metabolism might be a potential mechanism to explain the anti-metastatic action of PRM1201, as this gut-microbiota dependent effect involves downregulation of histone deacetylation and EMT. Methods: To investigate this possibility, clinical specimens were sequenced and the correlation between the antimetastatic efficacy of PRM1201 and the restoration of SCFA-producing bacteria was studied. To obtain solid causal evidence, a mouse metastasis model was established to detect the influence of PRM1201 on cancer metastasis. Specifically, 16S amplicon sequencing, ultra-high performance liquid chromatography -tandem mass spectrometry (UHPLC-MS/MS) analysis, and bacterial manipulation were used to examine the gut microbiotadriven anti-metastatic action of PRM1201. Results: Clinical data showed that PRM1201 increased both the number of SCFA-producing bacteria and generation of SCFAs in the feces of CRC patients. A positive correlation between the anti-metastatic efficacy of PRM1201 and the restoration of SCFAs observed. The animal experiments demonstrated that PRM1201 effectively blocked CRC metastasis in a dose-dependent manner. PRM1201 treatment modulated the composition of gut microbiota, and promoted the proliferation of beneficial SCFAs producers such as A kkermansia, Lachnospiraceae_NK4A136_group and Blautia , while simultaneously reducing the abundance of pathogenic bacteria like Escherichia-Shigella . In addition, PRM1201 led to augmentation of SCFAs content. Further results indicated that the anti-cancer metastatic mechanism of PRM1201 was linked to inhibition of histone deacetylation and suppression of epithelial-to-mesenchymal transition (EMT) in metastatic lesions. Microbiota depletion treatment and fecal microbiota transplantation (FMT) underscored the microbiota-dependent nature of this phenomenon. Moreover, this anti-colorectal cancer metastatic effect and mechanism of total SCFAs and single SCFA were also confirmed.

The incidence of nonalcoholic fatty liver disease (NAFLD) has been rising worldwide in parallel with diabetes and metabolic syndrome. NAFLD refers to a spectrum of liver abnormalities with a variable course, ranging from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH), eventually leading to cirrhosis and hepatocellular carcinoma. Pregnane X receptor (PXR), a member of the nuclear receptor superfamily, plays a prominent part in the regulation of endogenous metabolic genes in NAFLD. Recent studies have suggested that PXR has therapeutic potential for NAFLD, yet the relationship between PXR and NAFLD remains controversial. In this review, PXR is proposed to play a dual role in the development and progression of NAFLD. Its activation will aggravate steatosis of the liver, reduce inflammatory response, and prevent liver fibrosis. In addition, the interactions between PXR, substance metabolism, inflammation, fibrosis, and gut microbiota in non-alcoholic fatty liver were elucidated. Due to limited therapeutic options, a better understanding of the contribution of PXR to the pathogenesis of NAFLD should facilitate the design of innovative drugs targeting NAFLD.

Non-alcoholic fatty liver disease (NAFLD) is a chronic progressive disease that can progress to non-alcoholic steatohepatitis (NASH). Animal models are important tools for basic NASH research. Immune activation plays a key role in liver inflammation in patients with NASH. We established a high-trans fat, high-carbohydrate, and high-cholesterol, high-cholate diet-induced (HFHCCC) mouse model. C57BL/6 mice were fed a normal or HFHCCC diet for 24 weeks, and the immune response characteristics of this model were evaluated. The proportion of immune cells in mouse liver tissues was detected by immunohistochemistry and flow cytometry, Multiplex bead immunoassay and Luminex technology was used to detecte the expression of cytokines in mouse liver tissues. The results showed that mice treated with HFHCCC diet exhibited remarkably increased hepatic triglycerides (TG) content, and the increase in plasma transaminases resulted in hepatocyte injury. Biochemical results showed that HFHCCC induced elevated hepatic lipids, blood glucose, insulin; marked hepatocyte steatosis, ballooning, inflammation, and fibrosis. The proportion of innate immunity-related cells, including Kupffer cells (KCs), neutrophils, dendritic cells (DCs), natural killer T cells (NKT), and adaptive immunity-related CD3+ T cells increased; interleukin-1α (IL-1α), IL-1β, IL-2, IL-6, IL-9, and chemokines, including CCL2, CCL3, and macrophage colony stimulating factor (G-CSF) increased. The constructed model closely approximated the characteristics of human NASH and evaluation of its immune response signature, showed that the innate immune response was more pronounced than adaptive immunity. Its use as an experimental tool for understanding innate immune responses in NASH is recommended.

Objective The aim of this study was to investigate the clinical implication of serum alpha-fetoprotein（AFP）, alpha-fetoprotein-L-3 ratio（AFP-L3%） and protein induced by vitamin K antagonist-Ⅱ（PIVKA-Ⅱ） in early diagnosing and predicting prognosis of patients with primary liver cancer（PLC）. Methods A total of 87 patients with PLC, 79 patients with hepatitis B cirrhosis, 73 patients with chronic hepatitis B and 65 healthy persons were enrolled in our hospital between January 2016 and December 2018. All PLC patients underwent transcatheter arterial chemoembolization（TACE） and were followed-up for 3 years. Serum AFP and PIVKA-Ⅱ levels were detected by chemiluminescence immunoassay, and serum AFP-L3 level was assayed by immumofluorescence. The independent risk factors of impacting 3-year survival in patients with PLC were analyzed by Logistic regression analysis, and the prognostic value of serum AFP, AFP-L3% and PIVKA-Ⅱ levels was evaluated by the area under the receiver operating characteristic（ROC） curves（AUC）. Results Serum AFP, AFP-L3% and PIVKA-Ⅱ levels in patients with PLC were 402.5±95.3)μg/L,（12.9±3.1） and（824.5±82.1） mAU/mL, significantly higher than [（17.9±2.6）μg/L,（8.6±1.2） and（30.4±3.2）mAU/mL, P＜0.05] in patients with liver cirrhosis or [（20.3±6.4）μg/L,（5.4±0.9） and（29.8±3.0）mAU/mL, P＜0.05]in patients with CHB or [（2.2±0.1）μg/L,（2.7±0.4） and（26.3±3.4）mAU/mL, P＜0.05] in healthy individuals; serum AFP, AFP-L3% and PIVKA-Ⅱ levels in 52 dead patients with PLC one month after TACE were（447.1±71.2）μg/L,（14.1±2.2） and（883.9±50.8） mAU/mL, much higher than [（336.2±58.4）μg/L,（11.0±1.8） and（736.2±37.0）mAU/mL, respectively, P＜0.05] in 35 survivals; the univariate analysis showed that TNM staging, Child class, extrahepatic metastasis, serum AFP, AFP-L3% and PIVKA-Ⅱ levels were all influencing prognosis of patients with PLC（P＜0.05）, and the multivariate Logistic regression analysis showed that TNM staging ⅡI-IV, Child class C, extrahepatic metastasis, serum AFP ≥410.5μg/L, AFP-L3% ≥12.1 and PIVKA-Ⅱ≥807.2 mAU/mL were all independent risk factors for poor prognosis of patients with PLC（P＜0.05）; the ROC analysis showed that the AUC was 0.908 when combination of serum AFP, AFP-L3% and PIVKA-Ⅱ level detection in predicting the 3-year survival of patients with PLC, greatly superior to any parameter alone（the AUC were 0.763, 0.830 or 0.792, respectively, P＜0.05）. Conclusion The combination detection of serum AFP, AFP-L3% and PIVKA-Ⅱ levels could help diagnose and early predict prognosis of patients with PLC after TACE treatment.

Background The incidence of non-alcoholic fatty liver disease (NAFLD) has been on the rise in recent years, and there are no effective drugs to treat NAFLD; therefore, effective prevention and treatment of NAFLD have become a new challenge. Danggui Shaoyao Powder (DGSY) is a classic prescription commonly used in clinical practice and has been shown to reduce hepatic steatosis in patients with NAFLD. In addition, previous studies have shown that DGSY can alleviate hepatic steatosis and inflammation in NAFLD mice. Although clinical practice and basic studies have shown that DGSY is effective in NAFLD, high levels of clinical evidence are lacking. Therefore, a standardized RCT study protocol is required to evaluate its clinical efficacy and safety. Methods and analysis This study will be a randomized, double-blind, placebo-controlled, and single-center trial. According to the random number table, NAFLD participants will be randomly divided into the DGSY or placebo group for 24 weeks. The follow-up period will be 6 weeks after drug withdrawal. The primary outcome is the relative change in MRI-proton density fat fraction (MRI-PDFF) from baseline to 24 weeks. Absolute changes in serum alanine aminotransferase (ALT), liver stiffness measurement (LSM), body mass index (BMI), blood lipid, blood glucose, and insulin resistance index will be selected as secondary outcomes to comprehensively evaluate the clinical efficacy of DGSY in the treatment of NAFLD. The safety of DGSY will be evaluated by renal function, routine blood and urine tests, and electrocardiogram. Discussion This study will provide evidence-based medical corroboration for the clinical application of DGSY and promote the development and application of this classic prescription. Trial registration http://www.chictr.org.cn . Trial number: ChiCTR2000029144. Registered on 15 Jan 2020.

Non-alcoholic fatty liver disease (NAFLD) is a liver disorder characterized by abnormal accumulation of hepatic fat and inflammatory response with complex pathogenesis. Over activation of the pyrin domain-containing protein 3 (NLRP3) inflammasome triggers the secretion of interleukin (IL)-1β and IL-18, induces pyroptosis, and promotes the release of a large number of pro-inflammatory proteins. All of which contribute to the development of NAFLD. There is a great deal of evidence indicating that plant-derived active ingredients are effective and safe for NAFLD management. This review aims to summarize the research progress of 31 active plant-derived components (terpenoids, flavonoids, alkaloids, and phenols) that alleviate lipid deposition, inflammation, and pyroptosis by acting on the NLRP3 inflammasome studied in both in vitro and in vivo NAFLD models. These studies confirmed that the NLRP3 inflammasome and its related genes play a key role in NAFLD amelioration, providing a starting point for further study on the correlation of plant-derived compounds treatment with the NLRP3 inflammasome and NAFLD.

Non-alcoholic fatty liver disease (NAFLD) remains a common disease with a significant health and economic burden worldwide. The gut microbiota (GM) and bile acids (BAs), which play important roles in the gut-liver axis, have been confirmed to jointly participate in the development of NAFLD. GM not only regulate bile acids' synthesis, transport, and reabsorption by regulating other metabolites (such as trimetlyl amine oxide, butyrate), but also regulate dehydrogenation, dehydroxylation and desulfurization of bile acids. Meanwhile, disordered bile acids influence the gut microbiota mainly through promoting the bacterial death and lowering the microbial diversity. Although weight loss and lifestyle changes are effective in the treatment of NAFLD, the acceptability and compliance of patients are poor. Recently, increasing natural plants and their active ingredients have been proved to alleviate NAFLD by modulating the joint action of gut microbiota and bile acids, and considered to be promising potential candidates. In this review, we discuss the efficacy of natural plants in treating NAFLD in the context of their regulation of the complex interplay between the gut microbiota and bile acids, the crosstalk of which has been shown to significantly promote the progression of NAFLD. Herein, we summarize the prior work on this topic and further suggest future research directions in the field.

成纤维细胞生长因子21(FGF21)是成纤维细胞生长因子家族(FGF)中的一员,在维持机体能量代谢平衡等过程中发挥重要作用.近期两项FGF21类似物治疗非酒精性脂肪性肝病(NAFLD)的临床试验均达到各自的主要疗效评价终点.FGF21可以调控NAFLD相关的发病因素如糖脂代谢异常,还能改善炎症、抗应激损伤、抗纤维化和抑制NASH相关的HCC的发生.本文通过对FGF21类似物治疗NAFLD临床研究进展及相关机制研究进展进行综述,以全面介绍FGF21在NAFLD研究领域的进展.

Abstract We used cross‐sectional and longitudinal studies to comprehensively compare hepatic steatosis measurements obtained with magnetic resonance imaging–proton density fat fraction (MRI‐PDFF) and controlled attenuated parameter (CAP) in hepatic steatosis in adults with nonalcoholic fatty liver disease (NAFLD). A total of 185 participants with NAFLD and 12 non‐NAFLD controls were recruited. CAP and MRI‐PDFF data were collected at baseline from all participants and from 95 patients included in the longitudinal study after 24 weeks of drug or placebo intervention. Pearson correlation, linear regression, and piecewise linear regression analyses were used to evaluate the relationship between the two modalities. Linear analysis suggested a positive correlation between CAP and MRI‐PDFF (r = 0.577, p < 0.0001); however, piecewise linear regression showed no correlation when CAP was ≥331 dB/m (p = 0.535). In the longitudinal study, both the absolute and relative change measurements were correlated between the two modalities; however, the correlation was stronger for the relative change (relative r = 0.598, absolute r = 0.492; p < 0.0001). Piecewise linear regression analysis revealed no correlation when CAP was reduced by more than 53 dB/m (p = 0.193). Conclusions: We found a correlation between CAP and MRI‐PDFF measurements for grading hepatic steatosis when CAP was <331 dB/m. While the measured absolute change and relative change were correlated, it was stronger for the relative change. These findings have implications for the clinical utility of CAP or MRI‐PDFF in the clinical diagnosis and assessment of NAFLD.

Context Qushi Huayu decoction (QHD) has been clinically used for treating non-alcoholic steatohepatits (NASH). However, little is known about the effect of QHD on fatty acid beta-oxidation (FAO)-dependent lipid consumption. Objective To investigate the mechanism of QHD on FAO-related hepatic lipid accumulation. Materials and methods Male C57BL/6J mice were randomly divided into 5 groups (n = 8): normal diet and drinking water (CON), high-fat and high-carbohydrate diet (HFHC), QHD-L (2.875 g/kg), QHD-H (11.5 g/kg) and obeticholic acid (OCA) (10 mg/kg/day) groups. All mice freely consumed an appropriate diet for 18 weeks, and QHD was orally administered in the last 6 weeks. Measurements of general condition, hepatic histopathology, and JAK2/STAT3 signalling pathway were taken. Results QHD significantly improved NASH in mice, as reflected by improving serum glucolipid metabolism, decreasing enzymes activities, reducing hepatic triglyceride (HFHC: 70.07 +/- 2.81 mg/g; QHD-H: 34.06 +/- 5.74 mg/g) and ameliorating hepatic steatosis, inflammation in pathology. Further, both the mRNA and protein level of hepatic CPT-1A (p < 0.05), a rate-limiting enzyme of FAO, increased drastically following QHD treatment. Meanwhile, the content of hepatic ATP (p < 0.05) increased significantly after treatment with QHD. Further mechanistic results revealed that both the total protein and nuclear p-STAT3 in the liver were significantly down-regulated after QHD treatment. The protein level of hepatic p-JAK2 was significantly inhibited by QHD (p < 0.05 or p < 0.01). Conclusions QHD could attenuate lipid accumulation by increasing JAK2/STAT3/CPT-1A-related FAO, which provides a scientific basis for the clinical application of QHD in treating NASH.

门诊上经常会有患者拿着自己的B超检查结果咨询医生时,问到: “医生,为什么我最近饮食控制和运动坚持的都蛮好的,体重也有下降结果,可B超还是显示中度脂肪肝,我到底有没有好转呢,脂肪肝程度到底有没有减轻呢?” 答案当然是“不一定”! 辛辛苦苦坚持了好久,做检查却看不到什么改善,总会让患者心里感到淡淡的失落.仔细分析下,除了一些特殊情况患者脂肪肝确实没有改善外,可能还会因为检查做的不够精准!