The purpose of this study was to investigate the anti-injury effect and protective mechanism of hydrogen-enriched water in a rat model of acute liver injury induced by aflatoxin B (AFB). Healthy male Sprague-Dawley (SD) rats were randomly divided into control group, model group (AFB group) and hydrogen-enriched water treatment group (AFB+H group). The rat model of acute liver injury induced by AFB was established by single intragastric administration of AFB (2.0 mg/kg), and then the rats were treated with hydrogen-enriched water intragastrically. HE staining was used to observe the pathological changes of liver tissue. Blood samples were taken from vena cava to measure serum liver function indexes. Live tissue was sampled to detect malondialdehyde (MDA) and reduced glutathione (GSH) contents. Western blot was used to detect phosphorylation levels of MAPK signaling pathway proteins (ERK, JNK and p38 MAPK). The results showed that, compared with the AFB group, the AFB+H group exhibited increased body weights, alleviated acute liver injury, decreased activities of serum glutamic-pyruvic transaminase and glutamic oxaloacetic transaminase, as well as total bilirubin level in the serum. Meanwhile, hydrogen-enriched water decreased MDA content and increased GSH content in liver tissue. AFB-increased phosphorylation levels of ERK, JNK and p38 MAPK in liver tissue were down-regulated significantly by hydrogen-enriched water treatment. These results suggest that hydrogen-enriched water can alleviate liver injury induced by AFB, and its mechanism may be related to the reduction of oxidative stress and the inhibition of MAPK signal transduction pathway activation.
Aflatoxin B1 ; Animals ; Chemical and Drug Induced Liver Injury ; pathology ; prevention & control ; Deuterium Oxide ; therapeutic use ; Liver ; pathology ; MAP Kinase Signaling System ; Male ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: To investigate the effect of miR-204 on the invasion and metastasis of breast cancer by targeted regulation of HNRNPA2B1. METHODS: The bioinformatics database was used to obtain data of the expressions of miR-204 in breast cancer patients and the survival rate of the patients. RT-qPCR was used to detect the expression of miR-204 in breast cancer cell lines. The expression vector GV369-miR-204 was used to overexpress miR-204 in MDA-MB-231 cells. Transwell assay was performed to detect the effect of miR-204 on the migration and invasion ability of the breast cancer cells. The key genes (hub genes) of miR-204 were determined by bioinformatics method. A dual luciferase assay was used to analyze the targeting relationship between miR-204 and HNRNPA2B1. The expression of HNRNPA2B1 in MDA-MB-231 cells after miR-204 overexpression was detected by Western blotting, and Transwell assay was used to examine the changes in the cell invasion ability. RESULTS: The expression of miR-204 was decreased in both breast cancer tissues, and was significantly lower in breast cancer MDA-MB-231 cells than in MCF-10A cells ( < 0.05). The decreased expression of miR-204 was associated with poorer prognosis of breast cancer patients ( < 0.05). Upregulation of miR-204 in MDA-MB-231 cells significantly inhibited the invasion and migration of the cells ( < 0.05). Analysis of the data from the Starbase revealed that the expression of miR-204-5p was negatively correlated with the expression of HNRNPA2B1, and the expression of HNRNPA2B1 was increased in breast cancer patients ( < 0.05) in association with a poorer prognosis of the patients ( < 0.05). Dual luciferase assay demonstrated that miR-204 could bind to HNRNPA2B1 in a target-specific manner. Western blotting and Transwell assay showed that miR-204 significant inhibited the migration and invasion ability of breast cancer cells by targeting HNRNPA2B1 ( < 0.05). CONCLUSIONS miR-204 expression is decreased in breast cancer tissues and cells, and its overexpression can inhibit the invasion and metastasis of breast cancer cells by targeted regulation of HNRNPA2B1.
Breast Neoplasms ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; Neoplasm Invasiveness ; Neoplasm Metastasis

【Objective】 To study the molecular mechanism of 95 samples of serological ABO subtypes. 【Methods】 A total of 95 samples with discrepancy between forward and reverse blood grouping were subjected to serological confirmation, and genotyped by polymerase chain reaction with sequence-specific primers (PCR-SSP). For those subtype alleles could not be detected by PCR-SSP, ABO gene exon 1-7 sequencing and gene single strand sequencing were performed successively to determine the mutation site and the gene location. 【Results】 A total of 34 ABO alleles were detected in 95 samples. Five common ABO alleles (ABO^*A1.01, ABO^*A1.02, ABO^*B.01, ABO^*O.01.01 and ABO^*O.01.02) and 29 rare ABO alleles were identified, including 16 named alleles by ISBT (ABO^*A2.01, ABO^*A2.05, ABO^*A2.13, ABO^*A3.07, ABO^*AW.37, ABO^*AEL.05, ABO^*B3.01, ABO^*B3.05, ABO^*BW.03, ABO^*BW.07, ABO^*BW.27, ABO^*BEL.03, ABO^*cisAB.01, ABO^*cisAB.05, ABO^*BA.02, ABO^*BA.04) and 5 named alleles by dbRBC(A223, B309, Bw37, Bel09, Bw40)and eight unnamed alleles [ABO^*B.01+ 978C>A, ABO^*A1.02+ 248A>T, ABO^*B.01+ 125dupT, ABO^*B.01+ (98+ 1G>A), ABO^*A1.02/ABO^*B.01+ 1A>G, ABO^*A1.02/ABO^*O.01.01+ 28G>T, ABO^*A1.02/ABO^*B.01+ 538C>T, ABO^*A1.02/ABO^*O.01.01+ 797insT] .The last four samples could not be verified by single strand because of insufficient samples. In 95 samples, 76 samples (21 named alleles of ISBT and dbRBC) were identified by PCR-SSP, and the remaining 19 samples were identified by exon 1-7 sequencing of ABO gene, of which 8 were identified as unnamed alleles, and the remaining 11 samples were not identified as subtype alleles. 【Conclusion】 The molecular genetic mechanism of 95 serological ABO subtypes was revealed, and 8 rare novel alleles were identified. The detection of ambiguous blood groups is influenced by factors such as patient pathology and physiology, therefore the combination of serological testing and genetic testing is suggested for the identification of ABO subtype.

BACKGROUND: Derlin 3 (DERL3) is downregulated in colorectal cancer (CRC) samples. Its level is closely linked to lymphatic metastasis or distant metastasis rate in CRC patients. However, its biological behavior in lung adenocarcinoma were rarely reported. The aim of this study is to investigate the ectopic expression of DERL3 in lung adenocarcinoma tissues and its effect on the invasion and metastasis of lung adenocarcinoma A549 cell line to reveal the possible mechanism of invasion and metastasis of lung adenocarcinoma. METHODS: Lung adenocarcinoma microarray gene chip data included 3 cases of lymph node metastasis and 3 cases of lung adenocarcinoma tissue without lymph node metastasis. The GEDS and Kaplan-Meier plot queries the survival curve and expression level of DERL3. Western blot was used to detect the expression of DERL3 in lung adenocarcinoma cells. The efficiency of knockdown DERL3 gene was detected by Western blot assay. Transwell detected the number of cells passing through the basement membrane of the transwell. EDU assay detected cell proliferation ability. Western blot detected the expression of epithelial-mesenchymal transition related proteins E-cadherin and Vimentin. RESULTS: The microarray gene chip results showed that compared with lung adenocarcinoma tissues without lymph node metastasis, 1,314 mRNAs in lung adenocarcinoma tissues with lymph node metastasis were up-regulated, 400 mRNAs were down (P<0.05). The expression of DERL3 increased in lung adenocarcinoma (P<0.05). The results of survival curve showed that the lung cancer patients with high expression of DERL3 with poor prognosis (P<0.05). Western blot results indicated that plasmid transfection was successful. Knockdown of DERL3 suppressed the ability of proliferation, invasion and migration in A549 cells (P<0.05). After knockdown of DERL3, the expression level of Vimentin was decreased, while E-cadherin expression increased (P<0.05). CONCLUSIONS Knockdown of DERL3 inhibited the proliferation, invasion and metastasis of A549 cells.

BACKGROUND: MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression, influence cellular processes, and promote disease development. Variations in miRNA expression have been observed in many diseases, including hepatitis, cardiovascular disease, and cancer. The aim of this study is to investigate the effect of miR-144-3p on the invasion and metastasis of lung adenocarcinoma by targeting recombinant insulin receptor substrate 1 (IRS1). METHODS: The expression of miR-144-3p in patients with lung adenocarcinoma was queried through bioinformatics database. MirTarPathway was used to analyze the KEGG enrichment pathway of miRNA. The expression and plasmid transfection efficiency of miR-144-3p in lung adenocarcinoma cell lines were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Transwell assay was used to detect the changes of cell invasion and migration ability in different groups. Bioinformatics determined the key genes (Hub genes) of miR-144-3p; Double luciferase target assay was used to detect the mutual binding of miR-144 and IRS1. Western blot assay was used to detect the expression of IRS1 in different cell lines and the expression of after overexpression of miR-144. RESULTS: The expression of miR-144-3p in lung adenocarcinoma tissues was decreased, qRT-PCR results indicated that the expression of miR-144-3p in lung adenocarcinoma cell A549 was significantly decreased (P<0.05), and the overexpressed plasmid was successfully transfected (P<0.05). Overexpression of miR-144 decreased the ability of cell migration and invasion (P<0.05). The expression of IRS1 was up-regulated in lung adenocarcinoma tissues. Survival analysis showed that patients with lung adenocarcinoma with high IRS1 expression had a poor prognosis (P<0.05). Double luciferase assay results showed that miR-144 could specifically identify 3'-UTR of IRS1 and inhibit reporter enzyme expression (P<0.05). Western blot indicated that the expression of IRS1 was increased in A549 cells (P<0.05). After overexpression of miR-144, the expression level of IRS1 protein was decreased (P<0.05). Transwell experiment proved that miR-144-3p could inhibit invasion and metastasis of lung adenocarcinoma cells by targeting IRS1 (P<0.05). CONCLUSIONS MiR-144-3p inhibits the invasion and migration of A549 cells through targeted regulation of IRS1, thus playing an anticancer role in tumors.

Objective:To observe the clinical effect of modified Huangqi Guizhi Wuwu Tang on patient with lower-extremity arterial disease (LEAD) with deficiency of Qi and Yin and blood stasis syndrome, and study the antioxidant mechanism. Method:One hundred and twenty-eight patients were randomly divided into control group (64 cases) and observation group (64 cases) by random number table. Patients in control group was treated for controlling blood sugar, blood pressure and blood fat, and got probucol in the morning and evening, 0.5 g/time, 2 times/days, aspirin enteric-coated tablets for 3 months, 100 mg·d^-1, and alprostadil injection diluted with 10 mL normal saline for 15 days, 10 μg·d^-1, 1 time/day. A course of the treatment in control group was 15 days, and there were 4 courses. In addition to the therapy of control group, patients in observation group were additionally given modified Huangqi Guizhi Wuwu Tang, 1 dose/day, for 3 months. Before and after treatment, ankle brachial index (ABI) and toe branch index (TBI) were detected, and internal diameter of dorsal artery of foot, peak velocity and blood flow were detected by color Doppler ultrasound. Main symptoms and sign were scored. And levels of interleukin-1 (IL-1), Homocysteine (Hcy), tumor necrosis factor-α (TNF-α), high sensitive C reactive protein (hs-CRP), cystatin C (CysC), malondialdehyde (MDA), superoxide dismutase (SOD) and oxidized low density lipoprotein (OX-LDL) were detected. Result:According to the rank test, clinical effect in observation group was better than that in control group (P<0.05). And levels of ABI, TBI and SOD were higher than those in control group (P<0.01). The ameliorate of internal diameter of dorsal artery of foot, peak velocity and blood flow were better than those in control group, and scores of intermittent postscript, lower extremity pain, dorsalis pedis artery pulsation, skin color, skin temperature, numbness of limbs, swelling of extremities and the sign and levels of IL-1, Hcy TNF-α, hs-CRP, Cys-C and Ox-LDL were lower than those in control group (P<0.01). Conclusion:Modified Huangqi Guizhi Wuwu Tang can relieve symptoms and signs, lower limb vascular function and hemodynamic, with certain anti-inflammatory effect and oxidative stress. It can also reduce vascular endothelial cell injury, and relieve and postpone the progress of LEAD

Humans ; Neck Injuries/surgery* ; Carotid Artery Injuries/surgery* ; Neck ; Bone Screws/adverse effects* ; Carotid Artery, Common/surgery*

Hepatitis B virus (HBV) infection is a serious global public health problem. Chronic hepatitis B virus infection can cause health problems such as cirrhosis, liver metabolism disorders and hepatocellular carcinoma. Nucloes(t)ide analogues and interferon drugs used to treat chronic HBV infection do not completely eradicate covalently closed circular DNA (cccDNA) and integrated genome of HBV DNA, so that they cannot achieve the functional cure of chronic HBV infection. Currently, a series of drugs targeting the phases of HBV lifecycle and immunomodulators have entered clinical trials. Here, we review the current status of the therapeutic drugs as well as the recent advance of direct antiviral agents.

Trimethyltin chloride is a highly toxic substance, which is absorbed through respiratory tract, skin and digestive tract, with central nervous system injury as the main clinical manifestations, and can be accompanied by damage to various organs. In this paper, the treatment process of 3 patients with acute trimethyltin chloride poisoning was reviewed, and their clinical manifestations, auxiliary examination, diagnosis and treatment were analyzed. Three patients were misdiagnosed as mental abnormality, encephalitis, and hepatic encephalopathy in different hospitals in the early stage of medical treatment, suggesting that clinicians should pay attention to the occupational contact history of poisoned patients and conduct toxicant detection in time to avoid misdiagnosis and mistreatment.

ObjectiveTo investigate the effect of finasteride on the microvascular density (MVD) and the expression of the vascular endothelial growth factor (VEGF) in the seminal vesicle of rats.

METHODSForty male SD rats were randomly and equally divided into groups A, B, C and D, those in groups A and B fed with normal saline as the control and those in C and D with finasteride at 40 mg per kg of the body weight per day, A and C for 14 days and B and D for 28 days. Then the seminal vesicles of the animals were harvested for HE staining, measurement of MVD, determination of the expressions of CD34 and VEGF by immunohistochemistry, and observation of histomorphological changes in the seminal vesicle.

RESULTSThe expressions of CD34 in groups C and D were decreased by 6.7% and 15.8% as compared with those in A and B (P<0.01), and that in group D decreased by 9.3% in comparison with that in C (P<0.01). The expression indexes of VEGF in groups C and D were decreased by 6.9% and 14.1% as compared with those in A and B (P<0.01), and that in group D decreased by 9.0% in comparison with that in C (P<0.01).

CONCLUSIONSFinasteride can inhibit the expression of VEGF in the seminal vesicle tissue of the rat and hence suppress the angiogenesis of microvessels of the seminal vesicle.

Angiogenesis Inhibitors ; pharmacology ; Animals ; Antigens, CD34 ; metabolism ; Finasteride ; pharmacology ; Immunohistochemistry ; Male ; Neovascularization, Physiologic ; drug effects ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Seminal Vesicles ; blood supply ; drug effects ; metabolism ; Vascular Endothelial Growth Factor A ; metabolism