RESUMO
OBJECTIVE: To investigate the effects of tetrandrine on nuclear factor-kappaB (NF-kappaB) activity and proliferation of Diabetes Mellitus (DM) rats vascular smooth muscle cells (VSMCs). METHODS: DM models were established,the culture of DM and normal VSMCs were done by modified tissue-piece incoculztion; Inhibitory effect of Tetrandrine was determined by cell counting kit (CCK-8). Immunofluorescence laser confocal microscopy was used to estimate the effect of NF-kappaB in DM VSMCs with Tet. RESULTS: Tetrandrine inhibited the proliferation of DM and normal VSMCs,the IC50 value was (11.35 +/- 1.24) micromol/L and (28.01 +/- 4.35) micromol/L, respectively. Furthermore, Tetrandrine strongly inhibited the activation of NF-kappaB in DM VSMCs and reduced the nuclear translocation of NF-kappaB. CONCLUSION: Tetrandrine inhibits the proliferation of DM VSMCs more effectively than that of normal, the mechanism may be related to reducing NF-kappaB nuclear translocation.
Assuntos
Benzilisoquinolinas/farmacologia , Bloqueadores dos Canais de Cálcio/farmacologia , Proliferação de Células/efeitos dos fármacos , Diabetes Mellitus Experimental/patologia , Músculo Liso Vascular/efeitos dos fármacos , Stephania tetrandra/química , Animais , Células Cultivadas , Diabetes Mellitus Experimental/metabolismo , Masculino , Músculo Liso Vascular/metabolismo , NF-kappa B/efeitos dos fármacos , NF-kappa B/metabolismo , Plantas Medicinais/química , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , EstreptozocinaRESUMO
MicroRNAs (miRNAs) play important roles in cancer progression including gastric cancer. miR-485-5p is reported as a potential suppressor in breast cancer, but its expression, cellular function and clinic features in gastric cancer is not known. In our study, we found that miR-485-5p expression was down-regulated in gastric cancer cell lines. miR-485-5p could inhibit gastric cancer cell growth in vitro and in vivo. We also found that miR-485-5p suppressed gastric cancer cell metastasis and sphere formation. It was confirmed flotillin-1 (Flot1) as a direct target of miR-485-5p, and up-regulation of miR-485-5p could decrease expression of Flot1 in gastric cancer cells. Further investigation showed that ectopic expression of Flot1 partially reversed the inhibition effect of enforced miR-485-5p expression on the malignant phenotypes of gastric cancer cells. The low expression of miR-485-5p in gastric cancer tissues was related to advanced clinical features and poorer prognosis. Our study suggested that miR-485-5p could be a potential prognostic marker and functions as a tumor suppressor in human gastric cancer by post-transcriptionally targeting Flot1.