Objective To establish HPLC method for the determination of naringin in Jizhi droppills. Methods Kromasil C18 (4.6 mm?200 mm, 5 ?m) was used. The mobile phase was consisted of acetonitrile- 1% acetate solution (40∶60). The flow rate was 1.0 mL/min. The UV detection wavelength was at 283 nm. Results The linear range for naringin was 0.07～0.35 ?g, r=0.999 8. The RSD of precision test was 0.3%. The RSD of stability test was 2.3%. The RSD of repeatability test was 1.29%. The average recovery was 98.9%. Conclusion The method of precision and recovery was high, and stability and repeatability was good.

This study was aimed to investigate the effects of ursolic acid on human hepatic stellate cells (HSC-LX-2) proliferation and its mechanism.Different doses of ursolic acid were incubated with HSC-LX-2 cellin vitrof or 48 h.MTT was used for the detection of HSC-LX-2 cell proliferation.The expressions of PDGF-ERK signaling pathway associated proteins were measured by western blot.The results showed that the proliferation of HSC- LX-2 cells was inhibited by ursolic acid in a dose-dependent manner.The inhibition rate of 20,30 and 40μmol·L-1 of ursolic acid was 9.1%,42.3% and 62.6%,respectively.The IC50 was 35.2μmol·L-1.After incubated with ursolic acid for 48 h,protein levels of PDGF-R and p-ERK in 30 and 40μmol·L-1 group were significantly decreased when compared with the normal group (P<0.05 orP<0.01),except the ERK protein.It was concluded that ursolic acid can inhibit HSC-LX-2 cell proliferation.Its mechanism may be related to the blockage of PDGF-ERK signaling pathway.

Objective To discuss the intervention effects and mechanisms for Rapamycin on renal interstitial fibrosis in rats.Methods A total of 72 Wistar male rats were randomly divided into 3 groups,normal group(n =24) ,model group(n =24), treatment group (n =24).The model group and treatment group received adenine 200 mg/kg daily,and the treatment group was also given Rapamycin 5 mg/(kg·d) at the 8th day,the normal group was just given the same amount of normal saline for 6 weeks.In the end of the 2nd,4th and 6th week,8 rats in each group were sacrificed respectively.The expression of hepatocyte growth factor(HGF), transforming growth factor-β (TGF-β) and neutrophils gelatinases related apolipoprotein (NGAL) in each group were observed.The software of image analysis system was used for semi-quantitative analysis.Results HE and Masson staining results showed that the renal tubular were progressive swelling, and changed with interstitial fibrosis,atrophy and even necrosis in model group from 2 weeks to 6 weeks.The pathological changes of kidney were more ease in the treatment group compared with those in model group.Immunohistochemical staining results showed that HGF expression levels of renal interstitial tissue in model group and treatment group at the 2nd week were significantly higher than those of normal group(P ＜0.05), and were significantly decreased at the 4th week and 6th week (P ＜ 0.05);HGF expression levels of renal interstitial tissue in treatment group were significantly higher than those in model group (P ＜ 0.05).NGAL expression levels of renal interstitial tissue in model group and treatment group at the 2nd week were significantly higher than those in normal group(P ＜0.05) ,and were significantly decreased at the 4th week and 6th week(P ＜ 0.05);NGAL expression levels of renal interstitial tissue in treatment group were significantly higher than those in model group (P ＜ 0.05).TGF-β expression levels of renal interstitial tissue in model group and treatment group at the 2nd,4th,and 6th week were significantly higher than those in normal group (P ＜0.05) ,while TGF-β expression levels of renal interstitial tissue in treatment group were significantly lower than those in model group (P ＜ 0.05).Conclusion Rapamycin could improve the rat kidney tissue pathology, relieve renal tubular expansion, and slow progression of renal interstitial fibrosis, and has certain protective effect to the kidney.

Objective To explore the preliminary mechanism of mesenchymal stem cells (MSCs) in promoting prostate cancer proliferation in tumor inflammatory microenvironment.Methods From April 2013 to October 2013,MSCs pretreated with inflammatory cytokine IL-1α (MSCs (IL-1α)) and its culture supernatants mixed with RM-1 cells,which origined from C57BL/6 mice,were subcutaneously administered in the armpit area of C57BL/6 or BALB/c mice to establish homologous or heterologous transplant animal mode and to detect the tumor growth.Meanwhile the influence of MSCs on the proliferation of spleen cells was detected in vitro.Results In homologous transplant model,the relative tumor weight of prostate cancer cells prtreated with MSCs and MSCs (IL-1α) and their culture supernatant were (3.4 ± 0.2),(3.3 ±0.2),(4.9±0.5),and (5.2±0.6) g.The results were statistically significant (P＜0.05) compared with the control group (2.4±0.2) g.In heterologous model,the ratio of tumor formation of the pretreated groups were 50％,50％,80％ and 80％,respectively,compared with the control group of 0％.The results were statistically significant (P＜0.05).In proliferation experiments of spleen cells,the number of spleen cell pretreated with IL-1α were significantly lower than that in control group and unpretreated group (P ＜ 0.05).Conclusions MSCs pretreated with IL-1α could effectively promote the growth of prostate cancer cell in vivo.The reason may be due to inflammatory cytokines induce immune suppression of MSCs and then lead to immune escape of cancer cells.

Acetaminophen (APAP) overdose can induce liver injury and is the most frequent cause of acute liver failure in the United States. We investigated the role of p62/SQSTM1 (referred to as p62) in APAP-induced liver injury (AILI) in mice. We found that the hepatic protein levels of p62 dramatically increased at 24 h after APAP treatment, which was inversely correlated with the hepatic levels of APAP-adducts. APAP also activated mTOR at 24 h, which is associated with increased cell proliferation. In contrast, p62 knockout (KO) mice showed increased hepatic levels of APAP-adducts detected by a specific antibody using Western blot analysis but decreased mTOR activation and cell proliferation with aggravated liver injury at 24 h after APAP treatment. Surprisingly, p62 KO mice recovered from AILI whereas the wild-type mice still sustained liver injury at 48 h. We found increased number of infiltrated macrophages in p62 KO mice that were accompanied with decreased hepatic von Willebrand factor (VWF) and platelet aggregation, which are associated with increased cell proliferation and improved liver injury at 48 h after APAP treatment. Our data indicate that p62 inhibits the late injury phase of AILI by increasing autophagic selective removal of APAP-adducts and mitochondria but impairs the recovery phase of AILI likely by enhancing hepatic blood coagulation.