Objective To investigate the protective effects of FUZHENGJIEDU,a kind of Chinese herb on rats exposed to radon and it's daughter.Methods Twelve male SD rats were exposed with concentration of 40 000 Bq/m3 radon and the exposed dose was 120 work level month (120 WLM),and then all the rats were randomly divided into 2 groups.One group was 120 WLM group (positive control,n=6 ),the other group was FUZHENGJIEDU treatment group (120 WLM exposed rats were given FUZHENGJIEDU 5.0 g every day,n =6),meanwhile 6 rats which lived in the normal environment ( the concentration of radon and it's daughter was lower than 50 Bq/m3 ) as control group.The levels of tumor markers induding carcinoembryonic antigen ( CEA),neuron-specific enolase (NSE),CYFRA21-1 and p53 antibody were tested by ELISA.The rate of p16 gene methylation was measured by methylation-specific PCR (MSP).Results The levels of CEA and NSE in 120 WLM group were (396.62 ± 148.74) and (9.09 ±0.90) μg/L,respectively,significantly higher than those of control group (t =2.583,2.463,P ＜ 0.05).The levels of CEA and NSE in treatment group were (70.89 ±44.71) and (4.31 ±1.37) μg/L,respectively,remarkably lower than those of 120 WLM group (t =2.921,2.526,P ＜0.05 ).The concentrations of CYFRA21-1 and p53 antibody were not significantly different among the three groups (t =1.713,1.963,P ＞ 0.05 ).The rate of p16 gene methylation in BALF cells in 120 WLM group was 16.67％,but in control group and treatment group did not arise p16 gene methylation in BALF cells.Conclusions FUZHENGJIDU would decrease the levels of CEA and NSE and the rate of p16 gene methylation,and could exert it's protective effect on rats exposed to high concentration of radon.

The dosage-efficacy/toxicity relationship of the 50% alcohol extracts of Polygonum multiflorum was comparatively investigated on either normal or CCl4-induced chronic liver injury rats, by determining the general condition, serum biochemical indices and liver histopathology, coupled with the factor analysis. The dosages were 10 and 20 g raw materials per kg body weight. Compared with the normal control group, the normal high dose group showed significant increases of the serum alanine transaminase (ALT), total bilirubin (TBIL), high mobility group box 1 (HMGB-1) and interleukin-1β (IL-1β) (P < 0.05 or P < 0.01), as well the frequent incidences of inflammatory cell infiltration, hepatic sinus enlargement and fiber stripes formation in histopathological sections. Compared with the model control group, the model low dose group showed significant declines of serum ALT, aspartate transaminase (AST) and total bile acid (TBA) (P < 0.05), as well the alleviation of vacuoles of hepatocytes, but no amelioration of the inflammatory cell infiltration and fibrous tissue hyperplasia; moreover, the model high dose group showed significant degeneration declines of serum HMGB-1, tumor necrosis factor-α (TNF-α) and IL-1β (P < 0.05, P < 0.01), as well the evident alleviation of vacuoles degeneration of hepatocytes, inflammatory cells infiltration and fibrosis degree. The factor analysis showed that the low dosage treatment had almost neither injuring effect on the normal rats nor protective effect on the model rats; while the high dosage treatment showed observable injuring effect on the normal rats, expressed by the significant increases of the factor-1 (HMGB-1, TNF-α and IL-1β as the main contributors) and factor-2 (TBIL, ALT and TBA as the main contributors) relative to the normal control group. The liver protective effect of the high dosage treatment could be observed with the significant reduction of the factor-1, indicating the effective alleviation of the expression of inflammatory cytokines. In conclusion, it could illustrated the phenomenon of symptom-based prescription theory of Polygonum multiflorum on rat livers: the high dosage of the herb had either an injuring effect on normal rats, or a therapeutic effect on the rats with chronic liver injury.

The liver injury induced by Polygonum multiflorum Thunb. (PM) was investigated based on idiosyncratic hepatotoxicity model co-treated with lipopolysaccharide (LPS) at a non-hepatotoxic dose. Sprague-Dawley (SD) rats were intragastrically administered with three doses (18.9, 37.8, 75.6 g crude drug per kg body weight) of 50% alcohol extracts of PM alone or co-treated with non-toxic dose of LPS (2.8 mg·kg(-1)) via tail vein injection. The plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were assayed and the isolated livers were evaluated for histopathological changes. The dose-toxicity relationships of single treatment of PM or co-treatment of LPS were investigated comparatively to elucidate the idiosyncratic hepatotoxicity of PM. The results showed that no significant alterations of plasma ALT and AST activities were observed in the groups of solo-administration of LPS (2.8 mg·kg(-1), i.v.) or different dosage (18.9, 37.8 and 75.6 g·kg(-1), i.g.) of PM, compared to normal control group (P > 0.05); while significant elevations were observed in the co-administration groups of PM and LPS. Treatment with LPS alone caused slight infiltration of inflammatory cells in portal area but no evident hepatocytes injury. Co-treatment with LPS and PM (75.6 g·kg(-1), i.g.) caused hepatocyte focal necrosis, loss of central vein intima and a large number of inflammatory cell infiltration in portal areas. When further reduce the dosage of PM, significant increases of plasma ALT and AST activities (P < 0.05) were still observed in co-administration groups of LPS and PM (1.08 or 2.16 g·kg(-1)), but not in LPS or PM solo-administration groups. Nevertheless, the co-treatment of low dosage of PM (0.54 g·kg(-1)) with LPS did not induce any alteration of plasma ALT and AST. In conclusion, intragastric administration with 75.6 g·kg(-1) of PM did not induce liver injury in normal rats model; while the 2 folds of clinical equivalent dose of PM (1.08 g·kg(-1)) could result in liver injury in the LPS-based idiosyncratic hepatotoxicity model, which could be used to evaluate the idiosyncratic hepatotoxicity of PM.

To identify the regulatory region that are responsible for the expression of mPC-1, we have isolated and characterized the mPC-1 gene promoter. Sequence analysis of the mPC-1 5' -flanking region and a series of truncated constructs were performed, which were transiently transfected into the prostate cancer cell lines and non-prostate cancer cell lines and analyzed through Dual-luciferase reporter assay system. The relative activity of mPC-1 gene promoter was by far higher than pGL3-control containing SV40 promoter and enhancer and p61-PSA containing hPSA 6 kb promoter in AR (androgen receptor, AR ) -positive prostate cancer cell lines. The region from 599 bp to 449 bp of mPC-1 promoter might contain a negative regulatory element. The expression of mPC-1 1.1 kb fragment is mainly restricted into prostate cancer cell lines. The relative activity of mPC-1 1.1 kb 5'-flanking region was regulated by androgen. The results demonstrated that the 1.1 kb fragment of mPC-1 5' -flanking region was relatively strong and prostate cancer cell specific promoter region.The 1.1 kb promoter of mPC-1 gene might be well suited to prostate cancer gene therapy if the promoter was properly modified.

Objective:To investigate the expression of long non-coding RNA 00665 (LINC00665) in hepatocellular carcinoma (HCC) and its regulatory effect on angiogenesis of hepatocellular carcinoma cells and its potential molecular mechanism.Methods:HCC tissues and corresponding paracancerous tissues of 100 patients with HCC in the First Affiliated Hospital of Nanjing Medical University from May 2016 to April 2017 were collected, and the survival prognosis was compared. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of LINC00665 in HCC tissues and cells. The effect of LINC00665 overexpressed Hep-3B cells on the angiogenesis of human umbilical vein endothelial cells (HUVEC) was examined by tube formation assay and chick chorioallantoic membrane assay. Bioinformatics database predicted the downstream microRNA (miRNA) and target genes of LINC00665, and the relationship between LINC00665, miR-126-5p and vascular endothelial growth factor A (VEGFA) was verified by RT-qPCR, Western blot and dual-luciferase reporter gene assay.Results:The expression level of LINC00665 in HCC (6.5±2.8) was significantly higher than that in paracancer tissues (4.8±3.1), the difference was statistically significant ( t=4.12, P<0.001). According to the median LINC00665 expression level of 100 patients with HCC, the cumulative survival rate of LINC00665 high expression group ( n=50) was lower than that of LINC00665 low expression group ( n=50), and the difference was statistically significant (χ 2=3.79, P=0.008). After co-culture with LINC00665 group (Hep-3B cells overexpressing LINC00665), the length of HUVEC cell tubule formation was (596.0±22.3) μm, and the number of HUVEC cell tubules was (36.3±4.5), which were both higher than NC group with the tubule formation length (127.0±13.5) μm and the number (9.3±1.5) of HUVEC cells co-cultured with Hep-3B cells of control group, and the differences were statistically significant ( t=31.15, 9.82, P<0.001, P=0.001). The chick chorioallantoic membrane assay results were similar to tube formation assay. Western blot detected that the relative expression of VEGFA in LINC00665 group was higher than that in NC group, the difference was statistically significant ( t=7.15, P<0.001). StarBase and DIANA database were used to predict and screen LINC00665 downstream miR-126-5p. StarBase database was used to predict the binding sites of LINC00665/miR-126-5p/VEGFA axis. In dual-luciferase reporter gene assay, the fluorescence intensity of LINC00665 and VEGFA vector co-transfected with miR-126-5p mimics decreased. Conclusion:LINC00665 is highly expressed in HCC and is associated with poor prognosis in patients with HCC. LINC00665 promotes angiogenesis of HCC by regulating the miR-126-5p/VEGFA axis.