ABSTRACT
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.
ABSTRACT
Objective To explore the influence on the JNK signal transduction pathway by BaiHui-QuBin Scalp-acupuncture in rats of experimental acute intercerebral hemorrhage. Methods 192 healthy Wistar male rats were assigned into 3groups randomly:model group, model add pinprick group (to abbreviate:pinprick group), model add suppressor group(to abbreviate:suppressor group) ,containing 60 rats in each. All rats were induced be the intercerebral hemorrage model. Another 12 rats were assigned as the matched blank group. The pinprick group were acupunctured on the "Baihui" penetrating "Qubin". The influence surrounding the hamatoma of the proteinum expression of p-JNK of each group in deferent time phase point with the method of Western blot was observed. Results The results of expression of the proteinum p-JNK with the method of Western blot: all the rats after being made model appeared the phenomenon of the expression of p-JNK of rat's brain tissue surrounding the hematoma and increased to the peak in 2 days,but decreased gradually in 7days. In the same time phase point,compared with the model group,the expression of p-JNK of the pinprick group and the suppressor group were lower obviously (P ＜ 0.01). The pinprick group compared with the suppressor group, the expression of p-JNK showed no significant difference (P ＞ 0.05). Conclusion The therapy of BaiHui-QuBin Scalp-acupuncture could block the JNK signal tranaduction pathway, inhibit the expression of the proteinum p-JNK and so on have the function of protecting the nerve cell and inhibiting apoptosis.
ABSTRACT
Aim To investigate the hippocampal neuronal injury induced by ?-amyloid peptide ( A?) in rats and the candidate contribution of JNK signal transduction pathway to A? toxicity. Methods Rats were bilaterally injected with A?1 -40 into hippocampi CA1 area. The pathological changes,survival and apoptosis,and ultrastructure of hippocampal neurons,as well as p-JNK positive cells were observed by HE staining,Nissl staining,TUNEL staining,immunohistochemistry and transmission electron microscopy,respectively. Results Thepyramidal cells in hippocampus arranged loosely with decreased cell number. The gliacytes significantly proliferated. Significant apoptotic features were observed in CA1 ultrastructure. TUNEL-positive cells and p-JNK-positive cells significantly increased ( P