Objective:To explore the anti-fatigue effect of Tibet maca in mice. Methods: The mice were respectively given the powder or the alcohol extract of Tibet maca. The lactic acid concentration in blood, serum lactate dehydrogenase ( LDH) , the time of weight loading swimming and serum urea ammonia level after the exercise in the mice were detected, and the anti-fatigue effect of the powder and the alcohol extract of Tibet maca was compared. Results: After the 30-day feeding, the serum LDH activity of the mice taking the powder or alcohol extract of Tibet maca was obviously higher than that of the mice in the control group(P<0. 05), the time of weight loading swimming was significantly longer than that in the control group (P<0. 05), and the blood lactic acid concentration after the exercise was obviously lower than that in the control group (P<0. 05). Conclusion: Tibet maca can improve the time of weight loading swimming of mice, and reduce the level of serum urea ammonia after exercise and blood lactic acid concentration, sug-gesting the powder and alcohol extract of Tibet maca have obvious anti-fatigue effect.

Translational medicine is a totally new concept which could basically eliminate the barrier between basic medicine and clinical medicine and shorten the process of‘bench to bedside’Throughout the history of the diagnosis and treatment of acute pancreatitis,we found that changes of treatment concept at each historical stage were the results of‘translational medicine’under the technical and cognitive condition at that time.This paper elaborated on the important role of translational medicine based on the diagnosing and treating development of acute pancreatitis as well as discussed the medical teaching and research under the mode of translational medicine.

Objective To evaluate the migrating regulation and ultrastructure of the corneal epithelial stem cells in human fetuses. Methods We examined the corneal cryosections of 14-38 weeks of gestation. Hematoxylin-eosin staining showed the stratified corneal epithelium and the corneal epithelial stem cells were localized by mouse monocolonal antibody against human 64-kilodalton keratin (mAE5), and the ultrastructure of the corneal epithelial stem cells was observed. Results At 14 weeks of gestation, the corneal epithelium was composed of a single basal cells layer and 1-2 superficial squamous cells layers. Some superficial squamous cells were mAE5 positive in the limbus as well as the central and peripheral cornea. At 17-29 weeks of gestation, the limbus epithelium developed from 3 to 5 cells layers and the central region from 2 to 3 cells layers. mAE5 positive cells were found in the suprabasal layers of all 3 regions examined but not in the basal layer. At 33-38 weeks of gestation, the corneal epithelium consisting of 4-6 cells layers was morphologically mature. mAE5 immunoreaction showed the negative cells were confined to limbus basal layer. The ultrastructure of basal layer cells showed they had more heterochromatin in the nucleus, less organells in the cytoplasm and less desmosomes among them. Conclusion The migration of corneal epithelial stem cells in the human fetuses was from the whole layers to basal layer and confined to limbus region finally, and their ultrastructure was immature.

To compare the clinical effect of Qianliekang and finasteride in the treatment of benign prostatic hyperplasia to explore the effectiveness of traditional Chinese medicine for the therapy of benign prostatic hyperplasia. Methods:Totally 36 Wistar rats were selected, and then divided into 3 groups randomly with 12 ones in each, namely Qianliekang group, finasteride group and the control group. After 14 days of castration, the three groups were all treated with subcutaneous injection of 5 mg kg-1 testosterone propi-onate, and Qianliekang group was additionally treated with intragastric administration at 10-fold adult dose, finasteride group was trea-ted with intragastric administration at the dose of 0. 1 mg·kg-1 , and the control group was treated with the same amount of distilled water. The rats were sacrificed after the 21-day treatment, and the wet weight of prostate was determined, the prostate volume was measured and the pathological changes in prostate tissue were observed under a light microscope. Results:The wet weight of prostate in Qianliekang group and finasteride group was (0. 467 ± 0. 061) g and(0. 408 ± 0. 058) g, respectively, the prostate volume was (0. 371 ± 0. 059)ml and(0. 365 ± 0. 054)ml, respectively, and the above indicators were significantly lower than those in the control group(P<0. 05). Conclusion:Qianliekang can effectively inhibit benign prostatic hyperplasia in the model rats, and the mechanism may be related to the proliferation inhibition of prostate cells.

Objective Acute necrotizing pancreatitis (ANP) may cause lung injury.This study explores two factors that are associated with lung damage from ANP,the expression of tumor suppressor factor CYLD and nuclear factor-kappa B (NF-κB).Methods 72 adult Sprague-Dawley rats were randomly divided into 3 groups:sham operation,ANP,and GdCl3 treatment groups (n=24 for each group).A retrograde injection of 5％ sodium taurocholate into the biliopancreeatic duct of rats induced ANP,and the animals were killed 1,3,6,and 12 hours after the ANP induction.AMs were harvested by bronchoalveolar lavage technique,and TNF-a and IL-1β levels in bronchoalveolar lavage fluid (BALF) were evaluated.Lung tissue was checked with histological examinations,and the activity of NF-κB and CYLD in AM were measured by western blot.Results TNF-α and IL-1β secreted by AM were gradually elevated,peaked on the sixth hour,had maximums of (491.3 ±20.3)ng/L and (178.83±11.32)ng/L respectively,and decreased on the twelfth hour.The levels of TNF-α and IL-1β in the ANP group were significantly higher than the sham operation group (P＜0.05),and the GdC13 group levels were obviously lower than ANP group.In the sham operation group,the expression of NF-κB was low and CYLD was high.In the ANP group,when compared to the sham operation group,the expression of NF-κB rose after 3 hours and continued to rise with time progression (P＜0.05).In contrast,CYLD protein expression in the ANP group dropped after 3 hours and continued to gradually decrease (P＜0.05).The CYLD and NF-κB protein expression in GdCl3 groups had similar trends as the ANP group.GdCl3 group CYLD levels began to rise at 6 hours (P＜0.05),and NF κB levels began to fall at 1 hour (P＜0.05).The expression of NF-κB and CYLD possessed a negative correlation in both the ANP and GdCl3 groups (r =-0.918,r=-0.723,P＜ 0.01).Conclusions Therefore,in acute lung injury associated with acute pancreatitis,CYLD expression decreased with evident phases,such as a decrease in levels after 3 hours,and NF κB expression increased.Also,GdCl3 may be responsible for upregulation of CYLD expression and downregulation of NF-κB expression,and confirmed that CYLD had a negative effect on NF-κB.Perhaps GdCl3 could be used in the future to ameliorate the lung injury associated with ANP.

AIM: To study the effect of extract from Pongamia pinnata roots on anti-inflammation and analgesia and acute toxicity. METHODS: The models of mice ear edema induced by xylene and Cotton pellet granuloma in rats to observe the anti-inflammation effect of PRE via oral administration. The effect of PRE on analgesia was tested by measuring the latent period licking hind foot with the hot plate method and counting body twisting induced by acetic acid in mice. The acute toxicity of PRE was measured by the method of Bliss. RESULTS: PRE could significantly inhibit the ear edema caused by xylene in mice, granuloma hyperplasia caused by cotton in rats. It could significantly prolong the pain threshold on hot-plate in mice, reduce the writhing times in mice. The LD50 of PRE was 6. 371 8 g/kg, its 95% confident limit was 5. 408 4-7. 723 2 g/kg. CONCLUSION: PRE has obvious effect on anti-inflammation and analgesia and the lower acute toxicity.

AIM: To investigate the signal transduction mechanism of Chlamydia pneumoniae (Cpn) in down-regulating the expression of ATP binding cassette A1 (ABCA1) and ATP binding cassette G1 (ABCG1),the key molecules in cholesterol efflux and atherogenesis,from THP-1-derived macrophages. METHODS: Cpn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate (PMA) for 48 h,and were randomly allocated into 4 groups to incubate continually: control group,50 mg/L low density lipoprotein (LDL); Cpn infection group,Cpn (1×10~6 IFU) and 50 mg/L LDL; Cpn and SP600125 (a special JNK inhibiter) group,THP-1 macrophages were previously treated with different concentrations (1-20 μmol/L) of SP600125 for 1 h,and then infected with Cpn (1×10~6 IFU) and 50 mg/L LDL; SP600125 group,SP600125(20 μmol/L)and 50 mg/L LDL. The expressions of ABCA1/ABCG1 and peroxisome proliferator-activated receptor γ (PPARγ) from each group were detected then. The cholesterol efflux was detected by enzyme-fluorescence. The expressions of ABCA1/ABCG1 and PPARγ mRNA and protein were determined by RT-PCR and Western blotting,respectively. RESULTS: Cpn not only down-regulated the ABCA1/ABCG1 expression,but also down-regulated the expression of PPARγ,which regulated the ABCA1/ABCG1 genes transcriptions. However,the mentioned effects of Cpn infection were restrained by the special JNK inhibitor SP600125 in a dose-dependent manner. CONCLUSION: Chlamydia pneumoniae may down-regulate ABCA1/ABCG1 expression from THP-1-derived macrophages via JNK-PPARγ signal transduction pathway.

Objective To investigate the role of c-Jun N-terminal kinase (JNK) signal transduction pathway on the up-regulation of the expression of acyl-coenzyme A: cholesterol acyltransferasel (ACAT1) induced by Chlamydia pneumoniae (C. pn), and to discuss the mechanism of macrophages-derived foam cell formation induced by C. pn. Methods C. pn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA) for 48 h, and were randomly allocated into four groups to be incubated continually: control group, C. pn infection group, C. pn and SP600125 (a special JNK inhibitor)group and SP600125 group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellular cholesterol ester were detected by enzyme fluorescence analysis. The expressions of ACAT1 mRNA and protein were determined by reverse transcriptase polymerase chain reaction(RT-PCR) and Western blot, respectively. Results Compared with the control group, the expressions of ACAT1 mRNA and protein were up-regulated in C. pn infection group [(4.16±0.26) vs. (2.17±0.18), (1.20±0.10)vs. (0.61±0.03), both P<0.05], and C. pn-induced foam cell formation was observed. The expressions of ACAT1 mRNA and protein and the foam cell formation were inhibited by SP600125 in a concentration-dependent manner (r = - 0.92, P<0.05; r= - 0. 96, P<0.05, respectively). Conclusions The up-regulation of ACAT1 expression is induced by C. pn via JNK signal transduction pathway, which is involved in the mechanism of C. pn-induced macrophage-derived foam cell formation.

Objective:To investigate the effects of Chlamydia pneumoniae(Cpn) on SR-A1 and CD36 expression in THP-1-derived macrophages and role of c-Jun NH_2-terminal signal transduction pathway in the process.Methods:Cpn was propagated in Hep-2 cells.THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA)for 48h,and were randomly allocated into four groups to be incubated continually: control group;Cpn infection group;Cpn and SP600125(a JNK inhibiter)group and SP600125 group.Lipid droplets in cytoplasm were observed by oil red O staining.The contents of intracellular cholesterol ester were detected by enzyme-fluorescence.The expression of SR-A1 and CD36mRNA and protein were determined by RT-PCR and Western blot, respectively. Results:THP-1-derived macrophages infected with Cpn resulted in large accumulation of lipid droplets and foam cell formation when co-cultured with LDL.Meanwhile,the expression of SR-A1 mRNA and protein were up-regulated by Cpn infection (P<0.05).However,the expressions of CD36 mRNA and protein in THP-1-derived macrophages infected with Cpn were unchanged.Moreover,the up-regulation of SR-A1 and foam cell formation induced by Cpn could be restrained by the JNK inhibiter SP600125 in a dose-dependent manner,and SP600125 had little impact on the expression of CD36 in THP-1-derived macrophages infected with Cpn.Conclusion:The up-regulation of SR-A1 but not CD36 expression is involved in mechanisms of Cpn inducing foam cell formation.And Chlamydia pneumoniae up-regulates the expression of SR-A1 via the JNK signal transduction pathway.This may be a novel mechanism for the foam cell formation induced by Cpn.

Objective To investigate the mechanisms of Chlamydia pneumoniae (C. pn)-induced foam cell formation, the expression of ATP binding cassette transporter AI ( ABCA1 ) and perexisome prolif-erator-activated receptor γ (PPARγ) were examined. Methods THP-1 monneytes were induced into mac-rophages after the addition of 160 nmol/L phorbol myristate acetate (PMA) for 72 h. THP-1-dorived macro-phages when co-cuhured 50 mg/L low density lipoprotein (LDL) were designated randomly in four groups: control (uninfected) group, C. pn infection group, rosiglitazone + C. pn infection group and rosiglitazone group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellnlur choles-terol ester were detected by enzyme-flnoreseence. The expression of ABCA1, PPARγ, mRNA and protein were determined by RT-PCR and Western blot, respectively. Results C. pn down-regulated the expression of ABCA1, PPARγ at mRNA and protein levels in a concentration-dependent manner in THP-1-derived mac-rophages when co-incubated with LDL. Resiglitazone not only concentration-dependently alleviated the down-regulation of ABCA1 expression by C. pn infection (P<0.05), but also markedly suppressed the accumula- tion of lipid droplets and cholesteryl ester by C. pn at higher concentrations ( 10 and 20 μaol/L). Condu-sion C. pn induces foam cell formation by down-regulating the expression of ABCA1 via PPART pathway, which may provide a new evidence for the development and progression of atherosclerosis initiated by C. pn infection.