Objective: To explore the pharmacological basis and anti-inflammatory mechanism of persimmon leaf flavonoids（PLF） in preventing and treating oral ulcer. Methods: The analgesic and anti-inflammatory effects of PLF were evaluated by writhing test, pain threshold test, auricle swelling test and toe swelling test in mice. Moreover, based on rat oral uclcer model（acetic acid method）, the effects of PLF on the expressions of p38 mitogen activated protein kinases（p38MAPK）, phosphorylated p38MAPK（P-P38MAPK） and matrix metalloproteinase-2/9（MMP-2/9） in oral ulcer tissues were investigated by immunoboltting. Results: PLF could significantly reduce the number of writhing, increase the pain threshold, reduce the auricle swelling induced by xylene and inhibit the toe swelling induced by egg white. In addition, PLF could down regulate the expression of MMP-2/9 protein and inhibit the phosphorylation of p38MAPK. Conclusion: PLF has clear analgesic and anti-inflammatory effects. The therapeutic effects of PLF on oral ulcer may be through inhibiting MAPK signaling pathway and down-regulating expression of MMP-2/9.

Objective:To study the effect of thioredoxin domain containing protein 5 (TXNDC5)-peroxiredoxin 2 (Prx2) on the drug resistance of prostate cancer cells.Methods:Prostate cancer PC3 cells were cultured in vitro, treated with the chemotherapy drug cyclophosphamide (5, 10, 15 μmol/L) for 24 hours, and PC3 cells without any treatment was served as the control group. The expression levels of TXNDC5 in PC3 cells were detected by real-time fluorescent quantitative PCR (RT-qPCR) and Western blotting. PC3 cells with TXNDC5 knocking down were exposed by cyclophosphamide and CCK-8 was used to detect the cell viability of siTXNDC5 group and siNC group. The content of reactive oxygen free radicals was determined by reactive oxygen detection kit. PC3 cells and its parental cyclophosphamide-resistant ones with TXNDC5 knocking down were treated by 10 μmol/L cyclophosphamide and subjected for CCK8 assay. The expression of Prx2 in PC3 cells was detected by Western blotting after TXNDC5 was silenced. Prx2 expression was silenced in PC3 cells overexpressing TXNDC5, and cell viability and reactive oxygen free radical content were detected in Vec-Ctrl group, pcTXNDC5 group, siNC group, siPrx2 group and pcTXNDC5+ siPrx2 group. Results:Compared with the control group, cyclophosphamide treatment significantly increased the expression of TXNDC5 at mRNA and protein levels in PC3 cells. After PC3 cells were treated with cyclophosphamide (10, 15 μmol/L) for 12 h, compared with the siNC group, the cell viability in the siTXNDC5 group was significantly suppressed (0.44±0.08 vs. 0.74±0.10, t=3.647, P=0.031; 0.30±0.04 vs. 0.53±0.06, t=6.115, P=0.006). When PC3 cells were treated with 10 μmol/L cyclophosphamide for 6 and 12 h, compared with the siNC group, the production of reactive oxygen free radicals in the siTXNDC5 group was significantly increased (2.68±0.19 vs. 1.58±0.26, t=-6.027, P=0.005; 4.56±0.37 vs. 2.73±0.26, t=-6.995, P=0.003). When PC3 cells and its cyclophosphamide-resistant ones were treated with 10 μmol/L cyclophosphamide for 12 h, compared with the siNC group, the cell viability was significantly inhibited in the siTXNDC5 group. Western blotting analysis showed that the expression of Prx2 was significantly reduced when TXNDC5 was silenced. Silencing Prx2 could significantly attenuate the increase of cell viability and the decrease of reactive oxygen content resulting from TXNDC5 overexpression. PC3 cells were treated with 10 μmol/L cyclophosphamide for 12 h, and the cell viabilities of the Vec-Ctrl group, pcTXNDC5 group, siNC group, siPrx2 group and pcTXNDC5+ siPrx2 group were 0.52±0.07, 0.69±0.03, 0.56±0.05, 0.43±0.05, 0.58±0.07, respectively, and there was a statistically significant difference ( F=8.868, P=0.003). Furthermore, the cell viability in the pcTXNDC5+ siPrx2 group decreased significantly when compared to that of the pcTXNDC5 group ( P=0.045). The contents of reactive oxygen free radicals in the above 5 groups were 3.26±0.46, 2.09±0.49, 3.16±0.38, 4.62±0.26, 2.87±0.36, respectively, and there was a statistically significant difference ( F=16.037, P<0.001). The content of reactive oxygen radicals in the pcTXNDC5+ siPrx2 group was higher than that of the pcTXNDC5 group ( P=0.036). Conclusion:TXNDC5 can reduce the level of reactive oxygen free radicals in prostate cancer cells by regulating the expression of Prx2, so as to promote the drug resistance of prostate cancer cells.

目的 对口腔医学技术本科培养模式满意度进行调查,以满足社会对口腔医学技术专业人才的需求,提高专业人才就业稳定性.方法 对我院2014和2015级口腔医学技术专业本科生进行培养模式满意度调查,对调查结果 进行卡方检验.结果两个年级学生对实验课时安排和培养方案满意度有显著性差异,在选择与口腔医学技术专业相关职业就业方面也有显著性差异.结论 实验课时充足与否会影响学生对课程安排的满意度,进而影响学生的就业选择.

口腔医学是一门高度实践性的学科,创新精神和实践能力的培养是口腔医学教育的核心和精髓.本研究以创新教育理念为指导,结合口腔基础课程特点,探索构建以学生为本,以创新精神和创新能力培养为核心的口腔基础医学课程体系,在口腔基础课程学习阶段开展学科渗透性新教学实践,以期提高教学效果,培养实用型高级口腔人才.

目的 探讨柿叶黄酮在口腔溃疡大鼠中的抗氧化抗炎作用.方法 建立口腔溃疡大鼠模型(醋酸法),用桂林西瓜霜和不同剂量(20 mg·kg-1,40 mg·kg-1,80 mg·kg-1)的柿叶黄酮进行干预.观察血清和溃疡组织中的超氧化物歧化酶(SOD)和丙二醛(MDA)的变化;H-E染色观察组织病理形态学变化.结果 柿叶黄酮(20 mg·kg-1,40 mg·kg-1,80 mg·kg-1)可提高模型大鼠血清和溃疡组织中SOD活性、降低MDA含量(P<0.05);桂林西瓜霜和减轻溃疡组织的炎性浸润.结论 柿叶黄酮对醋酸诱导的口腔溃疡有一定的治疗作用,其机制与抗氧化损伤和降低炎症反应有关.

复发性口腔溃疡(以下简称RAU)属于口腔科常见的口腔黏膜疾病,并有高病发率、病发原因复杂、易复发、自愈性等特征,对病人日常生活造成了一定的影响.本文以RAU的病因病机分析为出发点,对目前国内外学者的研究成果进行了综述,并在此基础上探讨了治疗措施和新的研究进展,通过本文的研究希望能进一步明确RAU的病发机制,从而采取更为有效的临床治疗措施.

Objective To investigate the protective effect of.Persimmon leaf flavonoids(PLF) on the liver in alloxan-induced diabetic mice.Methods The diabetic mice model was established by tail vein injection of alloxan(60 mg/kg).The diabetic mice were divided into four groups treated with PLF0.5,2.5,5 g/kgand model control,while a normal conrol group was set up simultaneously.The drugs were given ig for two weeks.Three hours after the last treatment,the blood was taken by exposing the eye ball.separated from the serum,determination of the activity of ALT and AST;liver weight,liver index calculation;4% neutral formalin-fixed liver.The hepatic tissue was embedded with paraffin,sectioned,H-E staining,the histopathology was observed with microscope.Results Diabetic mice significantly increased the liver index;The activity of serum ALT and AST increased;The loss of normal hepatic lobular structure of cells,liver cells vacuolated degeneration and lymphocytic infiltration significantly.After treatment by PLF in diabetic mice,liver index and serum levels of AST and ALT decreased.Hepatocyte cord-like structure more clear,to reduce liver cell injury,reduced lymphocyte infiltration,included PLF 200 mg kg-1 best treatment Conclusion PLF can inhibit alloxan-induced diabetic mice hepatomegaly,the protection of liver function,reduce the pathological changes in liver tissue,and delay the progression of injury of liver induced by diabetes mellitus.