Objective To investigate whether vitamin D3 (VD3) can alleviate Helicobacter pylori (Hp) infection by reducing blood lipids and inhibiting the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway. Methods High-cholesterol mouse model and Hp infected mouse model were established. Each was treated with VD3 via oral administration for 8 weeks. Real-time quantitative PCR was used to detect the expression of vitamin D receptor (VDR), insulin-induced gene 2 (Insig-2), and gastrin mRNA. Western blot analysis was used to examine the expression of JAK, STAT3, and cyclooxygenase-2 (COX2) proteins in gastric tissues. Biochemical analyses were performed to measure serum cholesterol levels, and ELISA was utilized to evaluate serum gastrin, interleukin 6 (IL-6), and IL-8 levels, along with histopathological examination of liver and gastric tissues using HE staining. Results After oral administration of VD3, the levels of VDR and Insig-2 in mouse liver tissue significantly increased in the high cholesterol group and the high cholesterol combined with Hp infection group. And the expression of serum gastrin decreased. The expression of JAK, STAT3 in gastric tissues reduced, as did the expression of COX2. Serum cholesterol levels decreased, with no significant changes in IL-6 levels, but a reduction in IL-8 levels. Compared to the control group, the high cholesterol combined with Hp infection group showed reduced hepatic ballooning degeneration and alleviated gastric tissue inflammation. In addition, inflammation in gastric tissue was also reduced in the cholesterol group and the Hp infection group. Conclusion VD3 alleviates gastritis by enhancing the activity of VDR in liver tissues, blocking the JAK/STAT3 signaling pathway, and inhibiting the expression of inflammatory factors.

BACKGROUND Helicobacter pylori (H. pylori ) is the primary risk factor for gastric cancer (GC), the Wnt/β-Catenin signaling pathway is closely linked to tumourigenesis. GC has a high mortality rate and treatment cost, and there are no drugs to prevent the progression of gastric precancerous lesions to GC. Therefore, it is necessary to find a novel drug that is inexpensive and preventive to against GC. AIM To explore the effects of H. pylori and Moluodan on the Wnt/β-Catenin signaling pathway and precancerous lesions of GC (PLGC). METHODS Mice were divided into the control, N-methyl-N-nitrosourea (MNU), H. pylori + MNU, and Moluodan groups. We first created an H. pylori infection model in the H. pylori + MNU and Moluodan groups. A PLGC model was created in the remaining three groups except for the control group. Moluodan was fed to mice in the Moloudan group ad libitum. The general condition of mice were observed during the whole experiment period. Gastric tissues of mice were grossly and microscopically examined. Through quantitative real-time PCR (qRT-PCR) and Western blotting analysis, the expression of relevant genes were detected. RESULTS Mice in the H. pylori + MNU group showed the worst performance in general condition, gastric tissue visual and microscopic observation, followed by the MNU group, Moluodan group and the control group. QRT-PCR and Western blotting analysis were used to detect the expression of relevant genes, the results showed that the H. pylori + MNU group had the highest expression, followed by the MNU group, Moluodan group and the control group. CONCLUSION H. pylori can activate the Wnt/β-catenin signaling pathway, thereby facilitating the development and progression of PLGC. Moluodan suppressed the activation of the Wnt/β-catenin signaling pathway, thereby decreasing the progression of PLGC.

Abstract Background Currently, resistance to tyrosine kinase inhibitors, such as gefitinib, has become a major obstacle in improving the clinical outcome of patients with metastatic and advanced-stage esophageal squamous cell carcinoma (ESCC). While cell behavior can be modulated by long non-coding RNAs (lncRNAs), the roles of lncRNAs within extracellular vesicles (exosomes) are largely unknown. Therefore, we investigated the involvement and regulatory functions of potential lncRNAs enclosed in exosomes during formation of chemoresistance in human ESCC. Methods Gefitinib-resistant cell lines were established by continuously grafting TE1 and KYSE-450 cells into gefitinib-containing culture medium. LncRNA microarray assay followed by RT-qPCR were used to verify the differential expression of lncRNA Prostate Androgen-Regulated Transcript 1 (PART1) between gefitinib resistant and parental cell lines. RNA fluorescence in situ hybridization (FISH) was used to investigate whether extracellular PART1 could be incorporated into exosomes and transmitted to recipient cells. Subsequently, a series of in vitro assays and a xenograft tumor model were used to observe the functions of lncRNA PART1 in ESCC cells. A signal transduction reporter array, bioinformatics analysis, western blotting, and immunofluorescence were carried out to verify the regulation of PART1 and its downstream Bcl-2 signaling pathway. Results lncRNA PART1 was upregulated in gefitinib-resistant cells when compared to parental ESCC cells. It was found that STAT1 can bind to the promoter region of lncRNA PART1, resulting in its activation. Knockdown of lncRNA PART1 potently promoted the gefitinib-induced cell death, while elevated PART1 promoted gefitinib resistance by competitively binding to miR-129 to facilitate Bcl-2 expression in ESCC cells. In addition, extracellular PART1 could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating gefitinib resistance. Clinically, high levels of serum lncRNA PART1 in exosome were associated with poor response to gefitinib treatment in ESCC patients. Conclusions LncRNA PART1 promotes gefitinib resistance by regulating miR-129/Bcl-2 pathway, and may serve as a therapeutic target for ESCC patients.

抗生素在幽门螺杆菌中的耐药性越来越普遍，甚至出现了二重、三重、四重和五重耐药菌株，细菌可以通过多种方式适应抗生素施加的选择压力。外排泵的过表达有助于增加抗生素耐药性的产生，因此细菌可以在感染部位继续存在。除排出有毒物质外，外排泵还与持续形成和增加自发突变率有关，外排泵系统在幽门螺杆菌的耐药性中起着重要作用。本文就幽门螺杆菌的抗生素耐药性及其外排泵系统的研究进展作一综述，旨在为临床治疗耐药幽门螺杆菌感染提供一定思路。

BACKGROUND:Inflammation induced by Helicobacter pylori (H. pylori) infection is the basis for the pathogenesis of H. pylori. Butyric acid, a diet-related microbial-associated metabolite, is connected to inflammation, metabolic syndrome, and other diseases. Several studies have indicated the effects of sodium butyrate (SB) against bacteria; however, the effects of SB on the main virulence factors of H. pylori, H. pylori-induced inflammation, and gut microbiota composition remain unclear. MATERIALS AND METHODS:SB was supplemented in H. pylori coculture and administered to mice infected with H. pylori. The effects of SB intake on inflammation, gut microbiota composition, and short-chain fatty acids (SCFAs) in H. pylori-infected mice were assessed. RESULTS:The in vitro experiments demonstrated that SB not only inhibited the growth of H. pylori but also decreased the mRNA expression of CagA and VacA. SB intake reduced the production of virulence factors in H. pylori-infected mice, inhibited the IκBα/NF-κB pathway by reducing the expression of Toll-like receptors (TLRs), and reduced the production of TNF-α and IL-8. Further analysis demonstrated that H. pylori infection altered the relative abundance of the intestinal microbial community in mice. The level of SCFAs in the feces of H. pylori-infected mice was changed, although the intake of SB did not obviously change the level of SCFAs. CONCLUSIONS:Our study showed that SB may decrease H. pylori-induced inflammation by inhibiting the viability and virulence of H. pylori and may reduce inflammation in association with the gut microbiota in H. pylori-infected mice. This study may provide novel insights into the mechanisms by which SB, a diet-related microbial-associated metabolite, affects H. pylori-induced disease development.

This study was aimed to investigate the impact of probiotics on regulating the ROS/JNK signaling pathway their underlying mechanism of action in the treatment of nonalcoholic fatty liver disease. For this purpose, male C57BL/6 mice were randomly divided into three groups: control, probiotics, and model groups. Methionine and choline deficiency (MCD) diets were fed for four weeks to establish a NAFLD mouse model. Serum levels of ALT, AST, TC, and TG were detected. Moreover, the pathological changes of the liver and ileum tissues were observed by hematoxylin and eosin (H&E) staining, and the content of reactive oxygen species (ROS) in liver tissues was determined. In addition, the levels of D-lactic acid and plasma and small intestine diamine oxidase were measured to evaluate the effects of probiotics on the intestinal tract of NAFLD mice. The expression levels of p-JNK, Bax, and Caspase-3 were established to analyze the regulatory mechanism of probiotics on the JNK signaling pathway. We found that probiotics improve liver function, repair intestinal barrier and significantly suppressed oxidative stress, JNK phosphorylation. Moreover, the application of probiotics regulated the expression of signaling pathway-related proteins and promoted the intestinal barrier function repair and decreased intestinal permeability. The data above suggest that probiotics alleviate NAFLD, whose mechanism might be associated with the regulation of ROS/JNK signaling pathway and the suppression of oxidative stress and apoptosis.

由于肥胖和2型糖尿病发病率的快速上升,非酒精性脂肪性肝病(NAFLD)已成为发达国家常见的慢性肝病,是慢性肝病的主要病因之一.目前关于NAFLD的发病机制尚不明确,诊断与治疗也存在一定的局限性,最新研究表明piRNA在NAFLD的发病过程中起着重要作用.本文就NAFLD与piRNA的研究进展进行综述,旨在为NAFLD的发病机制、诊断及治疗提供新的方向.

Non-alcoholic fatty liver disease (NAFLD) has become a common health issue worldwide, and P-element-induced wimpy testis (PIWI)-interacting RNAs (piRNAs) have been shown to be differentially expressed in a variety of diseases. The aim of the present study was to investigate the potential relationship between piRNA and NAFLD. A NAFLD mouse model was established using a methionine- and choline-deficient (MCD) diet and methionine- and choline-sufficient (MCS) diet. Following this, mouse liver tissues were removed and stained with hematoxylin and eosin, and the levels of alanine aminotransferase, aspartate aminotransferase, total cholesterol and triglyceride were measured. Moreover, the liver tissues of the control and model groups were selected for piRNA gene chip analysis to identify piRNAs with differential expression in NAFLD. In addition, the differentially expressed piRNAs screened from the microarray were assessed by reverse transcription-quantitative PCR (RT-qPCR). piRNAs with potential research value were also selected for further analysis of target genes, using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways. The present study identified a total of 1,285 piRNAs with differential expression levels. The results indicated that in the model group, 641 piRNAs were upregulated, while 644 piRNAs were downregulated. Furthermore, piRNAs were enriched in 'cancer', 'Hippo signaling', 'Wnt signaling' and 'Mitogen-activated protein kinase signaling' pathways. The RT-qPCR results demonstrated that piRNA DQ566704 and piRNA DQ723301 were significantly upregulated in the model group, which was largely consistent with the analysis results of the piRNA arrays. Therefore, the results of the piRNA arrays and the further analyses in the present study were considered reliable. Collectively, the present results suggest that differentially expressed piRNAs exist in NAFLD and may affect the development of NAFLD via related pathways.

目的 研究piRNA在非酒精性脂肪性肝病(NAFLD)中的表达情况及两者之间的潜在关系.方法 将雄性C57BL/6小鼠随机分为对照组和模型组,每组10只.对照组进食蛋氨酸胆碱充足饲料,模型组进食蛋氨酸胆碱缺乏饲料.采用苏木精-伊红染色对肝组织切片行病理评估,并检测血清肝功能指标,包括谷丙转氨酶(ALT)、谷草转氨酶(AST)、甘油三酯(TG)和胆固醇(TC).使用piRNA基因芯片初筛肝组织中的差异piRNA,然后对差异piRNA行生物信息学分析,通过逆转录-定量聚合酶链反应进一步验证piRNA的表达.结果 模型组小鼠建立了有效的NAFLD模型.与对照组相比,模型组小鼠血清AST、ALT明显增高,TC、TG降低.模型组中共有1285个差异表达的piRNA,其中有641个piRNA发生上调,644个piRNA发生下调.生物信息学分析表明,差异表达的piRNA主要富集于hippo、Wnt、Cushing syndrome、FoxO、MAPK等信号通路.选择部分piRNA行RT-qPCR分析,其中piRNA-DQ566704、piRNA-DQ723301的结果与基因芯片分析结果基本一致.结论 在NAFLD发生发展过程中,确实存在piRNA的差异表达,然而piRNA影响NAFLD发展的具体机制还有待进一步研究.

Hepatocellular carcinoma (HCC) is a malignant tumor with extensive metastasis. Changes in the tumor microenvironment provide favorable conditions for tumor metastasis. However, the role of changes to the tumor microenvironment in HCC metastasis is yet to be elucidated. The Gene Expression Omnibus expression profile GSE5093 consists of 20 noncancerous tissues surrounding HCC tissues, including 9 metastasis-inclined microenvironment samples with detectable metastases and 11 metastasis-averse microenvironment samples without detectable metastases. The present study assessed 35 HCC samples to verify the results of chip analysis. In total, 712 upregulated and 459 downregulated genes were identified, with 1,033 nodes, 7,589 edges and 10 hub genes. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that the differentially expressed genes were significantly enriched in 'cell-cell adhesion', 'cell proliferation' and 'protein binding'. The top 10 hub genes were identified via a protein-protein interaction analysis. The 3 most significant modules were identified from the protein-protein network. Moreover, an association between hub genes and patient prognosis was identified. In conclusion, these candidate genes and pathways may help elucidate the mechanisms underlying HCC metastasis and identify more options for targeted therapy.

随着社会的发展及人们生活水平的日益提高,非酒精性脂肪肝病(NAFLD)逐渐成为威胁人类健康及增加经济负担的最常见的慢性肝病之一.其呈现出发病率持续增长且年轻化的趋势,与之伴随的心血管疾病风险事件也逐渐升高.目前基于NAFLD的诊断手段各有优势,但都存在一定的局限性,并且尚没有治疗NAFLD的有效药物.本文主要从NAFLD的诊断和治疗进展方面进行综述,为NAFLD的临床诊治提供相关的参考.

OBJECTIVE To investigate the effects of equal concentration of Helicobacter pylori suspension on gastric mucosal infection in mice by different gavage methods. 
 Methods: Six-week-old male C57BL/6 mice were infected by a suspension of Brucella broth containing the same amount of NCTC11637 Helicobacter pylori suspension by A, B, C, and D methods. For method A, the mice were intragastrically administered with Helicobacter pylori suspension (0.2 mL per mouse), once two day for 5 times; for method B, the mice were intragastrically administered with Helicobacter pylori (0.2 mL per mouse) once a day for 5 times; for method C, the mice were perfused with 0.4 mL per mouse of Helicobacter pylori suspension on the first day, then once a day and 0.2 mL per mouse for 3 times; for method D, the mice were administrated with 0.4 mL per mouse Helicobacter pylori suspension on the first day, 0.2 mL per mouse every other day for 3 times. For method E, the mice received equal amounts of normal saline. The mice were killed at 2, 4, and 6 weeks after gavage. The gastric mucosa was detected by rapid urease test for Helicobacter pylori infection, and gastric mucosa was taken for HE staining to observe the degree of infection.
 Results: After 2 weeks of gavage, the infection rates of the mice in A, B, C, and D group were 33.3%, 50.0%, 66.7%, and 33.3%, respectively. The degree of inflammation infection was as following order: C group>B group>D group>A group>E group. The infection rates of mice after 4 weeks of gavage in the A, B, C, and D groups were 50.0%, 83.3%, 83.3%, and 66.7%, respectively. The degree of inflammation infection was as following order: C group>B group>D group>A group>E group. After 6 weeks of gavage, the infection rate in A, B, C, and D groups was 100%, while the degree of inflammation infection was as following order: C group>D group>B group>A group>E group.
 Conclusion: At the acute stage of Helicobacter pylori infection, different gavage methods show different infection rates in mice, and the degree of inflammation is different. At the chronic stage, different gavage methods display the same infection rate in mice with different degree. The gavage method that 0.4 mL Helicobacter pylori suspension on the first day, then once a day and 0.2 mL for 3 times is most conducive to Helicobacter pylori colonization in the gastric mucosa of mice. This method can induce the the most seriou inflammatory infection and is beneficial to the successful establishment of the Helicobacter pylori infection model.

The aim of the present study was to investigate the role of microRNA-21 (miR-21) in regulating the classical WNT/beta-catenin signaling pathway by targeting low-density lipoprotein-related receptor 6 (LRP6) in non-alcoholic fatty liver disease (NAFLD). For this purpose, we established a NAFLD model by feeding C57BL/6J mice a methionine-choline-deficient diet. Antagomir-21 was then injected via the tail vein, and the expression levels of WNT/beta-catenin signaling pathway-related proteins, such as LRP6, glycogen synthase kinase-3 beta (GSK3 beta), p-beta-catenin, beta-catenin and the downstream protein, peroxisome proliferator-activated receptor gamma (PPAR-gamma), and lipid metabolism-related genes, including sterol regulatory element-binding transcription factor 1c (SREBP1c), fatty acid synthase (FAS), carnitine palmitoyl transferase 1 alpha (CPT1 alpha) and adenosine 5-monophosphate (AMP)-activated protein kinase alpha (AMPK alpha), were detected. The results revealed that in the NAFLD model, LRP6 expression was negatively associated with miR-21 expression. After antago-nizing the expression of miR-21, the protein level of LRP6 was increased. In addition, the WNT/beta-catenin signaling pathway was activated, and lipid accumulation and inflammation were alleviated in the liver. However, the expression of PPAR-gamma was not inhibited following the upregulation of the WNT signaling pathway. Taken together, the results of this study demonstrate that the inhibition of miR-21 expression can alleviate NAFLD by targeting LRP6 to activate the WNT/beta-catenin signaling pathway.

OBJECTIVE: Gastrointestinal tumors are malignant tumors with high morbidity. Mitochondria! serine hydroxymethyltransferase 2 (SHMT2) is a key enzyme in the synthesis of serine and glycine, which has prognostic and therapeutic value for many malignant tumors. However, the role of SHMT2 in gastric cancer (GC), esophageal cancer (ESCC), and colorectal cancer (CC) has not been clarified. PATIENTS AND METHODS: The expression of SHMT2 was detected in GC, ESCC, and CC by immunohistochemistry and reverse real time transcription-polymerase chain reaction. The relationships between SHMT2 expression and clinicopathologic characteristics, recurrence-free survival (RFS), and disease-specific survival (DSS) were analyzed by the survival analysis and correlation analysis. RESULTS: The positive expression rate of SHMT2 in GC, ESCC, and CC was 74.1%, 69.2%, and 71.7%, respectively. Patients with high expression of SHMT2 had a worse prognosis. In GC, high SHMT2 expression had positive correlation with lymph node metastasis (p=0.005) and histological grade (p=0.002). In ESCC, high SHMT2 expression had positive correlation with pT classification (p=0.033) and pM classification (p=0.029). In CC, high SHMT2 expression had positive correlation with tumor size (p=0.004), lymph node metastasis (p=0.035), TNM stage (p=0.007), and histological grade (p=0.020). Notably, SHMT2 expression was an independent prognostic factor for RFS and DSS in GC, ESCC, and CC (p<0.05). CONCLUSIONS: SHMT2 is upregulated in GC, ESCC, and CC. The high expression of SHMT2 is correlated with gastrointestinal tumors progression, and poor prognosis, which is a potential new target for the diagnosis and treatment of gastrointestinal tumors.

Objective To investigate the infection rate and risk factors of Helicobacter pylori in healthy people in Luzhou. Methods From May 2017 to May 2018, the number of physical examinations for Helicobacter pylori infection was 18, 684 in the Affiliated Hospital of Southwestern Medical University of Ganzhou, the Affiliated Hospital of Southwestern Medical University and Cangzhou People 's Hospital and Jixian People's Hospital.C14, C13 breath test or Hp antibody positive could be considered as Helicobacter pylori infection. Eight hundred people were randomly selected to conduct a telephone survey. The survey content included general information, living habits, blood type and personal and family gastrointestinal related past medical history. Results The HP infection rate of the medical examination population in Cangzhou City was 31.6％, the male HP infection rate was32.4％ (3788/11836) , the female HP infection rate was 30.4％ (2086/6848) , and the male HP infection rate was higher than that of the female (P = 0.025). Univariate analysis showed that gender, BMI, drinking, drinking water, frequent eating, family members and the previous digestive tract diseases, and previous history of oral disease were risk factors for Helicobacter pylori infection. Results of multivariate logistic analysis showed Male, BMI, drinking, drinking water, eating out often, family members and the digestive tract disease, and a history of oral disease were risk factors for Helicobacter pylori infection. Conclusion BMI, drinking water, and eating out in the medical examination population of Quzhou City, family members, the digestive tract diseases and previous history of oral disease are risk factors for Helicobacter pylori infection.

The prevalence of non-alcoholic fatty liver disease (NAFLD) has been increasing in recent years. Previous studies have suggested that micro (mi)RNAs may be involved in the pathogenesis of NAFLD. To investigate the role of miRNAs in rat NAFLD, a total of 16 male Sprague Dawley rats were randomly divided into a control group and a model group. Rats in the control group were fed a normal diet for 12 weeks, whereas the rats in the model group were fed a high-fat and high-sugar diet for 12 weeks. Following this, the animals were sacrificed and liver tissues were rapidly removed to investigate the severity of NAFLD. Blood samples were collected to investigate liver function, in addition to total cholesterol, total triglyceride and fasting plasma glucose levels. Total RNA from three fresh liver samples per experimental group was extracted for subsequent miRNA gene chip analysis using GeneChip miRNA 4.0 to investigate differentially expressed miRNAs, and miRNA expression was further verified via reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Compared with the control group, the results revealed that there were 10 differentially expressed miRNAs in the model group, five of which were overexpressed and five of which were underexpressed compared with the control group. The results of the RT-qPCR analysis revealed that miR-182, miR-29b-3p and miR-741-3p were significantly overexpressed in the model group compared with the control group, which was largely consistent with the results of the microarray analysis. The results suggested that the differentially expressed microRNAs demonstrated in the present study may be involved in the pathogenesis of NAFLD; however, the mechanism underlying the differential expression of miRNAs in NAFLD requires further investigation.

Nonalcoholic fatty liver disease (NAFLD) is a chronic disorder characterized by hepatic fat accumulation and abnormal lipid metabolism. Although miR-21 has been implicated in nonalcoholic fatty liver disease, it is unknown whether miR-21 could function as a therapeutic target. Here, we perform transfection analysis of miR-21 mimic or control mimic to evaluate the effects of miR-21 expression levels on human HepG2 nonalcoholic fatty liver cells. We used siRNA techniques to knock down miR-21 in HepG2 and control 293T cell lines, and then monitored lipid production and the expression levels of genes involved in lipid metabolism. The effects of miR-21 expression levels on LDL receptor-related protein 6 (LRP6) expression were evaluated using qRT-PCR and western blot analyses. Luciferase reporter assays were conducted to confirm the effects of miR-21 expression levels on LRP6. The results indicated that transfection of miR-21 mimic induced changes in the expression levels of lipogenic enzymes, including acetyl-CoA carboxylase 1 (ACC1), stearoyl CoA desaturase (1SCD1), sterol regulatory element-binding protein 1 (SREBP1), and liver X receptor alpha (LXRα). Transfection of miR-21 mimic suppressed the transcription and translation of LRP6 at the mRNA and protein levels, whereas miR-21 knockdown increased the expression levels of LRP6. Transfection of miR-21 mimic in HepG2 cells also induced lipid production and triggered the expression of critical lipid metabolic enzymes. These data suggest that mutation of miR-21 may be a new therapeutic strategy to treat nonalcoholic fatty liver diseases by targeting endogenous LRP6.

Pyruvate kinase M2 (PKM2), a key protein in glucose and lipid metabolism, has been reported to be related to carcinogenesis in various malignancies. However, its roles in hepatocellular carcinoma with cirrhotic liver (CL) and hepatocellular carcinoma with non-cirrhoticliver (NCL) haves not been investigated. In our study western bloting, qRT-PCR and immunohistochemistry were performed to evaluate the clinical significance of PKM2 protein expression in CL and NCL. The results revealed that PKM2 protein expression was significantly higher in HCC tissues than in their adjacent non-tumour tissues. The high expression rates of PKM2 were more frequently noted in CL (45. 6%) than in NCL (31. 9%) tissues. High PKM2 expression in CL and NCL tissues was significantly associated with vascular invasion (P = 0.002 and P = 0.004, respectively) and intrahepatic metastasis (P < 0.001 and P = 0.019, respectively). Importantly, Kaplan–Meier survival analysis showed that the disease-specific survival (DSS) and recurrence-free survival (RFS) were lower in CL with high PKM2 expression than in NCL with high PKM2 expression (P = 0.003 and P = 0.003, respectively). Overall, high PKM2 expression was more frequently found in CL than in NCL, and PKM2 overexpression was associated with poor survival rates in patients with CL and NCL.

PURPOSE::To investigate the effect of curcumin on visfatin and zinc-α2-glycoprotein (ZAG) expression levels in rats with non-alcoholic fatty liver disease (NAFLD).METHODS::Fifty-six male rats were randomly divided into a control group (n=16) and model group (n=40) and were fed on a normal diet or a high-fat diet, respectively. Equal volumes of sodium carboxymethyl cellulose (CMC) were intragastrically administered to the control group for 4 weeks. At the end of the 12th week, visfatin and ZAG protein expression levels were examined by immunohistochemistry. Visfatin mRNA levels were measured by semi-quantitative reverse transcription polymerase chain reaction.RESULTS::Compared with the control group, the model group showed significantly increased expression of visfatin in liver tissue (P < 0.01) and significantly decreased expression of ZAG (P < 0.01). These effects were ameliorated by curcumin treatment.CONCLUSIONS::Visfatin and zinc-α2-glycoprotein may be involved in the pathogenesis of NAFLD. Treatment of NAFLD in rats by curcumin may be mediated by the decrease of visfatin and the increase of non-alcoholic fatty liver disease.