AIM: To study the relation between prolon ge d survival of skin allograft by chuan-ke-zhi (CKZ, drug of Chinese herbal) and C D4+CD25+ regulatory T cells (CD4+CD25+ Tr) in mice. METHODS: Skin allograft and isograft model in mice were establi shed and CKZ was administered by intraperitoneal injection. To observe its influ ence on survival of the graft, three color fluorescent staining together with fl ow cytometry was used to analyze the change of CD4+CD25+ Tr. RESULTS: The survival of skin allograft in CKZ group was signifi cantly prolonged compared to control group, (19.5?2.3) days and (10.2?2.2) days, respectively, P0.05). CONCLUSION: CKZ has an effect of prolonging the survival of skin allograft. Enhancement of CD4+CD25+ Tr might be one of the mechanisms under lying its immunosuppressive effect.

0.05) compared with control group at 1 h and 3 h; while ~FL 1 in DEX group at 5 h (660.91?72.95) was significant lower (P

AIM: To study the effect of ERK inhibition on the mitochondrial potential change in dexamethasone (DEX)-induced thymocyte apoptosis. METHODS: ERK activity was inhibited by PD098059 (PD), and 4 experimental groups were set: control, PD only, DEX and PD+DEX. Annexin V-FITC/PI double staining flowcytometry was used to detect apoptotic cells at time points of 3 h, 5 h and 7 h. JC-1 staining flowcytometry was adopted to examine mitochondrial membrane potential (△?m) at time points of 3 h, 7 h and 11 h. RESULTS: By stimulation with 1 ?mol/L DEX, the apoptotic rates of mouse thymocytes at 3 h, 5 h and 7 h were (19.63?0.35)%, (41.84?1.67)% and (67.00?2.43)%, respectively, and had significantly difference from control group (4.98?0.39)%, (6.08?0.33)% and (9.31?0.34)% (P0.05). At 3 h, 7 h and 11 h, the rates of low △?m cells were (21.23?1.43)%, (55.34?1.78)% and (70.88?2.87)%, significantly higher than that in control group (P0.05). CONCLUSION: DEX induces mouse thymocyte apoptosis at least partly through ERK pathway, and ERK inhibition has an important biological significance during this process.

AIM: To study the effects of ultraviolet (UV) on mitochondrial functions and apoptosis in HaCaT cells.METHODS: After irradiation by UV at low dose(UVA 2 J/cm~2,UVB 10 mJ/cm~2) and high dose(UVA 6 J/cm~2,UVB(30 mJ/cm~2),) HaCaT cells were cultured for 15 hours.Flow cytometry was used to measure mitochondrial membrane potential,mitochondrial mass and apoptotic rate.Annexin V-FITC/PI staining of apoptotic cells was analyzed by laser confocal microscopy.RESULTS: After UV irradiation,cell proportion with low mitochondrial membrane potential increased with irradiation doses.The proportion of control group,low dose group and high dose group were 7.94%?1.02%,25.87%?4.55% and 39.27%?5.32%,respectively.Cells proportion with low mitochondrial mass increased with irradiation doses.The proportion of control group,low dose group and high dose group were 15.19%?1.58%,40.36%?4.41% and 68.79%?5.46%,respectively.The hypodiploid peaks of DNA content analysis represented the apoptotic rate of HaCaT cells.The apoptotic rate of control group,low dose group and high dose group were 1.82%?0.51%,30.16%?5.47% and 58.49%?5.98%,respectively.To analyze the cells apoptosis by staining with annexin V-FITC and PI,the results were consistent with those of DNA content analysis.Cells in control group showed almost no positive staining cells.Single annexin V-FITC positive cells in low dose group and double positive cells in high dose group were predominant,respectively.CONCLUSION: UV irradiation induces HaCaT cell mitochondrial depolarization,as well as mitochondrial mass loss.These changes are related to cell apoptosis.

AIM: To study the changes of mitochondrial membrane potential(△?m) and mitochondrial mass in apoptosis of Jurkat cells induced by camptothecin(CPT).METHODS: Jurkat cells were treated with CPT.Annexin V-FITC/propidium iodine(PI) double stainig was used to detected early stage of apoptosis and PI staining for analyzing the cell cycle.Jurkat cells were stained by annexin V-PE/DiOC_6(3) to detect changes of △?m.The mitochondrial mass was measured by cytometry with NAO staining.RESULTS: 6 h after treated with 10 ?mol/L CPT,the rate of early apoptotic cells(22.59?1.04)% had significantly difference compared with control group(3.93?0.73)%(P0.05).Apoptotic peak appeared obviously after treated with CPT,the percentage of late apoptotic cells(13.58?0.97)% had distinctly difference compared with control group(3.18?0.51)%(P

In recent years， neurotoxicity caused by traditional Chinese medicine （TCM） has frequently occurred and has become one of the important factors restricting the development and application of TCM. TCM contains active components and its dosage-effect relationship is the key to determine its pharmacological activity and toxic effects. Among them， the endogenous toxic components include alkaloids， glycosides， diterpenoids， animal and plant toxic proteins and heavy metals， and so on； exogenous toxic components mainly refer to some harmful elements and pesticide residues during the cultivation， processing， transportation and storage of medicinal materials that are not synthesized by themselves. Effect on the processes such as oxidative stress， inflammation， ion exchange， and energy metabolism may be important mechanisms of TCM-induced neurotoxicity. Neural cells， myelin cells， axons and neurotransmitter systems are common targets of TCM-induced neurotoxicity. In the future， we can use modern research methods and big data mining means to establish a safety evaluation mode of “toxic symptoms-poisoning dose-toxic original agent-detoxification scheme” with the basic component group of toxic substances as the core， so as to provide support for development and clinical intervention of neurotoxic traditional Chinese medicine.