OBJECTIVE:To study the in vitro uptake of Resibufogenin(RBG)lactic acid glycolic acid copolymer-water solu-ble vitamin E (PLGA-TPGS) in human liver cancer HepG2 cells,mouse ascites-type lymphatic metastasis of tumor HCa-F cells, and the toxicity on HepG2 cells. METHODS:RCPTN loading RBG and coumarin-6(C6)were prepared. Fluorescent inverted mi-croscope was used to observe the in vitro uptake by RCPTN HepG2,HCa-F cells. It was divided into negative control group,blank PLGA-TPGS nanoparticles(EPTN)group,5-fluorouracil solution(FS)group,RBG solution(RS)group,RBG/PLGA nanoparti-cles(RPN)group and RPTN group. WST-1 was conducted to investigate the optical density at 450 nm wavelength of HepG2 cells after 24,48,72 h incubated by FS,RS,RPN and RPTN with different final concentrations (1.25,2.5,5,10,20 μg/mL);the cell viability (CV) and half inhibitory concentration (IC50) were calculated. RESULTS:RCPTN distributed around the nucleus of HepG2,HCa-F cells. CV was decreased by RBG concentration increased in RPN group and RPTN group,and decreased by time prolonged;compared with FS group,CV in RPTN group was decreased(P<0.05 or P<0.01). IC50 of HepG2 cells incubated by FS,RS,RPN and RPTN was decreased by time prolonged,ordered by RS>FS>RPN>RPTN;IC50 incubated by RPN and RPTN for 48,72 h was obviously less than that of FS and RS(P<0.05 or P<0.01). CONCLUSIONS:RPTN can deliver RBG in-to HepG2,HCa-F cells,showing inhibition effect on HepG2 cells which is stronger than RPN,RS and FS.

Objective To observe the effects of total flavone from litchi chinensis sonn (TFL) on the liver function in-cluding p16 protein, pro collagen type 3 (PC3) and pro collagen typeⅠ(PCⅠ) in model rats with liver fibrosis induced by bile duct ligation. Methods Forty rats were randomly divided into four groups:sham operation (SO) group, bile duct liga-tion (BDL) group, TFL group and silibinin (SIL) group. Rats were gavaged with saline (5 mL·kg-1·d-1) in SO and BDL group, rats were gavaged with TFL (200 mL·kg-1·d-1) in TFL group and rats were gavaged with SIL (5 mL·kg-1·d-1) in SIL group for four weeks. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin direct (BILD) and bilirubin total (BILT) were detected in four groups. The liver tissues were stained by HE and Masson methods. The ex-pression levels of p16, PC3 and PCⅠin liver tissues were determined by Western blot assay. Results The serum levels of ALT (44.6 IU/L±8.0 IU/L), AST (103.8 IU/L±18.1 IU/L), BILD (0.76 μmol/L±0.28μmol/L) and BILT (1.48μmol/L±0.35μmol/L) were lower in SO group. There was a higher level of ALT in BDL group (147.4 IU/L±86.3 IU/L) than that of TFL group (92.9 IU/L±47.3 IU/L). The serum level of ALT was higher in AST group (362.7 IU/L±106.6 IU/L) than that of TFL group (290.1 IU/L ± 171.7 IU/L) and SIL group (250.2 IU/L ± 54.9 IU/L). The serum level of BILD was lower in BDL group (99.71μmol/L±40.87μmol/L) than that of SIL group (137.01μmol/L±38.86μmol/L). The serum levels of BILD and BILT were significantly lower in TFL group (81.48μmol/L±47.50μmol/L, 106.64μmol/L±61.04μmol/L) than those of SIL group (P<0.05). There were small amount of new bile duct and no obvious cells degeneration, small amount of infiltration of in-flammatory cells and collagen deposition in TFL group. The liver fibrosis improved significantly in TFL group than that of BDL group. There were more new bile duct in hepatic portal area in SIL group than those of TFL group. The expression levels of p16, PC3 and PCⅠwere significantly higher in BDL group than those of TFL group. The expression level of PC3 was significantly lower in BDL group than that of SIL group. The expression level of PCⅠwas significantly higher in BDL group than that of SIL group (P<0.05). There was no significant difference in the expression level of p16 between BDL group and SIL group. The expression levels of PC16 and PC3 were significantly lower in TFL group than those of SIL group (P<0.05). There was no significant difference in the ex-pression level of PCⅠbetween TFL group and SIL group. Conclusion TFL can improve the liver function in model rats with choles-tatic liver fibrosis and reduce liver fibrosis, which may be related with inhibitory effects on the expressions of p 16, PC3 and PCⅠ.

【Objective】 To analyze the clinical data of prostate cancer patients with normal PSA level confirmed with transperineal prostate biopsy or transurethral prostate surgery, in order to improve the diagnostic level of this disease. 【Methods】 The clinical data of 6 patients were retrospectively analyzed. The age,clinical manifestations, body mass index (BMI),prostate specific antigen density (PSAD),blood triglycerides,blood cholesterol,color ultrasound imaging,magnetic resonance imaging (MRI),pathological types and Gleason scores were analyzed. The clinical characteristics and high-risk factors were summarized. 【Results】 Two cases were confirmed with prostate biopsy and four after prostate resection. Three patients had high blood triglycerides, three were negative for bone imaging, and the other three were not examined. PSAD was 0.017 to 1.215. Color ultrasound indicated that two cases had irregular morphology, two uneven echo, and one both irregular morphology and uneven echo; all six cases had calcification. In the three cases who received MRI, two had PIRADS4 nodules, one had PIRADS5 nodules, invasion of seminal vesicle, rectum, posterior wall of urinary bladder,bilateral thickening of NVB, and lymph nodes enlargement. Pathology suggested prostatic acinar adenocarcinoma in five cases, four of which had a Gleason score of 3+3=6 and one had 5+5=10; one case suggested a high-grade neuroendocrine carcinoma. 【Conclusion】 The clinical detection rate is low for prostate cancer with normal PSA. The biopsy indications should be determined by combining the characteristics and high-risk factors to improve the detection rate.

ObjectiveTo observe the effect of Coptidis Rhizoma and Ophiopogonis Radix on renal tissue injury and epidermal growth factor receptor （EGFR）/phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway in rats with diabetic nephropathy （DN） and explore its possible mechanism of delaying DN. MethodThirty-six male Wistar rats were randomly divided into a normal group （6 rats） and a model group （30 rats）. The model group was fed with a high-fat and high-sugar diet combined with streptozotocin （STZ） to establish a rat model of type 2 diabetes. After the successful preparation of the model， the rats were randomly divided into the model group， low， medium， and high dose groups of Coptidis Rhizoma and Ophiopogonis Radix （100， 200， 400 mg·kg^-1）， and metformin group （200 mg·kg^-1）. After administration， the levels of fasting blood glucose （FBG）， 24 h urine protein （24 h-UTP）， creatinine （SCr）， urea nitrogen （BUN）， and uric acid （UA） were detected. Hematoxylin-eosin （HE） staining and Masson staining were used to observe the pathological changes of renal tissue in rats. Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were used to detect the related protein expression of EGFR， PI3K， and Akt and their mRNA expression levels in the renal tissue of rats in each group. ResultsCompared with the normal group， the levels of FBG， SCr， BUN， UA， 24 h-UTP， and kidney index in the model group were significantly increased （P<0.01）， most renal tubular epithelial cells were necrotic， and the content of collagen in glomeruli was significantly increased （P<0.01）. Compared with the model group， the above indexes of rats in each administration group were improved to varying degrees. The FBG， SCr， BUN， UA， 24 h-UTP， and kidney index of rats in each dose group and metformin group were significantly decreased （P<0.01， P<0.05）. The necrosis degree of renal tubular epithelial cells was reduced， and the fibrosis area was decreased （P<0.01）. There related protein and mRNA expressions of EGFR， PI3K， and Akt were significantly increased （P<0.05， P<0.01）. ConclusionCoptidis Rhizoma and Ophiopogonis Radix can alleviate renal tissue injury in rats with DN， and their mechanism may be related to the regulation of the EGFR/PI3K/Akt signaling pathway.