ABSTRACT
Psoriasis is a non-infectious chronic inflammatory skin disease. It′s acknowledged that interleukin (IL)-17 signaling pathway dominantly drives the development of psoriasis. Recently, the role of neuro-immune axis in psoriasis has attracted widespread attention. Lidocaine, a local anesthetic, has ability to block the conduction of nerve impulses, while its therapeutic efficacy on psoriasis remains to be confirmed. Here, we evaluated the therapeutic efficacy of topical application of compound lidocaine cream (LIDO) on imiquimod (IMQ)-induced mouse psoriasis model. Animal welfare and experimental procedures follow the regulations of the Ethics Committee of China Pharmaceutical University. The psoriasis area and severity index (PASI) scoring was used to evaluate the severity of psoriasis-like symptoms. Hematoxylin-eosin staining was used to examine histopathological changes and epidermal thickness was measured. Ki67 immunofluorescence staining was used to evaluate the proliferation of keratinocytes. The relative mRNA expression of inflammatory cytokines (including Il17, Il22, Il23 and Il36) in skin was measured by real-time quantitative PCR. Results show that IMQ-induced increases in the PASI score, epidermal thickness, number of Ki67+ cells and the mRNA expression of inflammatory cytokines are significantly alleviated by topical application of LIDO, whose therapeutic efficacy is also better than that of the positive control drug calcipotriol. Our study suggests that LIDO could be used for psoriasis treatment.
ABSTRACT
Objective To investigate the met ho ds of isolation,culturing and passaging of neural stem cells originated from ra t embryonic brains.Methods The neural stem cells were obtained from the brain tissue of rat embryos.They were cultured and passaged with serum-free medium.T hey were identified with Nestin and stained with NF68,GFAP,and GalC after diff erentiation.Results We cultured the neural stem cells through several passages .With the help of serum,they differentiated to neurons,astrocytes and oligode ndrocytes.Conclusion The neural stem cells derived from rat embryonic brains a re able to proliferate and multiplepotent for differentiation.
ABSTRACT
Objective To investigate the interactions and effects of Helicobacter pylori (H.pylori) and non steroidal anti inflammatory drugs (NSAID) on the proliferation of gastric epithelial cells in vitro. Methods After co culturing of gastric cancer cell line AGS cells with H.pylori and/or NSAID (indomethacin and aspirin) for 48 hours, the cell proliferation and proliferating cell nuclear antigen (PCNA) were examined by MTT assay and Western blot. Results cagA positive H.pylori strain NCTC11637, but not cagA negative H.pylori strain NCTC12908, had the effect of enhancing gastric epithelium cell proliferation. However, the effect of proliferation was dependent on the density of H.pylori . It was demonstrated that low density (range from 3.2?10 4 CFU/ml to 4?10 6 CFU/ml) of bacteria suspensions resulted in proliferative effect, while high density (more than 2?10 7 CFU/ml) resulted in inhibition. Besides, indomethacin and aspirin inhibited cell proliferation in a dose dependent manner. Moreover, when AGS cells were incubated with cagA positive H.pylori and NSAID, inhibition rather than proliferation was observed. cagA positive H.pylori strains up regulated the expression of PCNA while indomethacin and aspirin down regulated the level of PCNA expression. Meanwhile, the expression of PCNA was also reduced significantly when AGS was co cultured with H.pylori and NSAID. Conclusions The results indicated that gastric epithelium cell proliferation was associated with different H.pylori strains and its density. cagA positive H.pylori strain is prone to increase cell proliferation, but cagA negative H.pylori strain has no such effect. NSAID can inhibit gastric epithelial cell proliferation and reverse such effect caused by H.pylori.