The Mechanism Behind the Anti-Apoptotic Effects of TNK on Islet β Cell in Type 2 Diabetic ZDF Rats / 世界科学技术-中医药现代化

This study aimed to investigate the anti-apoptotic effects of Tangnaikang (TNK) on islet β cells in Zucker diabetic fatty (ZDF) rats.Six male fa/+ ZDF rats were took as the control group,while other thirty male fa/fa ZDF rats were divided into five groups at random:the model group,the metformin group,the high-,mediumand low-dose TNK groups,depending on their body weight and random blood glucose.Prior to the administration,fasting blood glucose and fasting insulin were measured by drawing blood with inner canthusl.Materials were prepared when administered for six weeks.Fasting blood glucose and fasting insulin were detected again.When the sections of the rat pancreatic tissue were embedded,the morphological changes of the islet were observed via HE staining,and the apoptosis of islet β cell were observed using TUNEL.Positive expression of Caspase-3,the transduction enzyme of cell death signal,was tested by immunohistochemical method.It was found that the fasting blood glucose of the (fa/fa) ZDF rats in the high-,medium-and low-dose TNK group was significantly improved after administration (P ＜ 0.01).The serum insulin of rats in the high-,medium-and low-dose TNK group arised compared with the model group,while the high-and low-dose TNK group showed differences in a statistical sense.Compared with the model group,the HOMA-IR of all the treatment group decreased,while significant difference was presented between the high-dose TNK group and the metformin group.HE staining showed that the morphology of the islet β cell of the rats in all the treatment group was improved.The results of TUNEL showed significantly apoptotic changes on islet β cell of the fa/fa ZDF rats.Compared with the model group,the positive expression of TUNEL in the metformin group and the high-dose TNK group were significantly reduced (P ＜ 0.05).The result of immunohistochemistry method showed that the protein levels of Caspase-3 in the metformin group and the high-dose TNK group decreased (P ＜ 0.05).In conclusion,it was demonstrated that TNK effectively reduced the apoptosis of islet β cells in fa/fa ZDF rats,which presented a protective effect.

Neuroprotective effect of Liuwei Dihuang decoction on cognition deficits of diabetic encephalopathy in streptozotocin-induced diabetic rat.

ETHNOPHARMACOLOGICAL RELEVANCE: Liuwei Dihuang decoction (LWDHD) is a well-known prescription of traditional Chinese medicine (TCM) and consists of six crude drugs including Rehmannia glutinosa Libosch. (family: Scrophulariaceae), Cornus officinalis Sieb. (family: Cornaceae), Dioscorea oppositifolia L. (family: Dioscoreaceae), Paoenia ostii (family: Paeoniaceae), Alisma orientale (G. Samuelsson) Juz (family: Alismataceae) and Poria cocos (Schw.) Wolf (family: Polyporaceae). It has been used for the treatment of "Kidney-Yin" deficiency syndrome in clinic in China for a long time. Recent studies found that LWDHD had a potential benefit for the treatment of diabetic complications. The aim of the present study is to investigate the neuroprotective effect of LWDHD on memory and cognition deficits in streptozotocin (STZ)-induced diabetic encephalopathy (DE) rats. MATERIALS AND METHODS: Adult male Sprague Dawley (SD) rats were fed with high-glucose-fat diet for 50 days and then received an intraperitoneal injection of STZ (40 mg/kg) to induce DE model. Morris water maze test was used to evaluate the memory and cognition capability of DE rats. Choline acetyltransferase (ChAT), acetylcholinesterase (AChE), Na(+)-K(+)-ATP enzyme, iNOS and GSH kits were used to determine their activities or content in hippocampus. TUNEL staining, immunohistochemistry and Congo red staining were conducted to evaluate the apoptosis, caspase-3 protein expression, insulin-like growth factors 1 (IGF-1) and brain derived neurophic factor (BDNF) expressions, as well as Aß deposition. RESULTS: The treatment with LWDHD (1 and 2g/kg, p.o., once daily, 30 days) could significantly reduce the escape latency time and path length, and obviously enhance the spent time in the target quadrant and platform crossings in Morris water maze test compared with model group (P<0.05, P<0.01). LWDHD could also significantly decrease the level of fasting blood glucose, increase Na(+)-K(+)-ATP enzyme and ChAT activities, enhance remarkedly GSH level while decrease significantly AChE and iNOS activities in hippocampus (P<0.05, P<0.01). Furthermore, TUNEL staining, Congo red staining and immunohistochemistry showed that LWDHD significantly improved the expressions of IGF-1 and BDNF, attenuated the neural apoptosis, overexpression of caspase-3 and Aß deposition in the hippocampus and cerebral cortex of STZ-induced DE rats (P<0.01). CONCLUSION: Our findings suggested that LWDHD had a neuroprotective effect on DE rats. LWDHD may be of benefit in the treatment of DE.

Research on induced apoptosis of recombinant human adenovirus-p53 injection in patients with oral leukoplakia / 肿瘤研究与临床

Objective To probe the biological effect of multiple intraepithelial injections of recombinant adenovirus-p53(rAd-p53)on inducing the apoptosis in patients with dysplastic oral leukoplakia.Methods 18 patients clinically and histopathologically diagnosed as dysplastic oral leukoplakia were recruited for this study.Intraepithelial injections of rAd-p53 were administered.Immunohistochemistry was used to examine the protein expression of p53 and bcl-2.TUNEL was performed to detect apoptotic cells.Results In the post-treatment patients,p53 protein expression were significantly enhanced(100 ％,18/18),yet bcl-2 protein presented low expression(17 ％,3/18).Statistical analysis revealed the expression of p53 protein had a negative correlation with that of bcl-2 protein(r =-0.837,P ＜ 0.01).15 post-treatment samples (83 ％)were detected obvious apoptotic cells,especially in the samples that were strong p53-positive(r =0.684,P ＜ 0.01).Conclusion Intraepithelial injections of rAd-p53 can induce apoptosis for patients with dysplastic oral leukoplakia.It may be a promising treatment for oral leukoplakia.