Journal of ethnopharmacology · 2009
Bushen Ningxin Decoction pharmacological serum promotes the proliferation and suppresses the apoptosis of murine osteoblasts through MAPK pathway.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang YuDong, Cui Kemi, Zhao Hong, Li DaJin, Wang WenJun, Zhu Ying
Аннотация
AIM: In the present study, we investigated the effects of pharmacological serum from the ovariectomized mice treated with Bushen Ningxin Decoction (BSNXD) on cell growth and etoposide-induced apoptosis of mouse osteoblasts (OBs).
METHODS: The ovariectomized BALB/c mice serving as a postmenopausal osteoporosis model were treated with BSNXD for 12 weeks. The serum from the mice was collected and applied to the cultivation of the calvaria OBs of newborn BALB/c litters. Cell proliferation was measured by methyl thiazolyl tetrazolium (MTT) assay. Apoptosis rate was analyzed by Annexin V-FITC/PI flow cytometry (FCM) and the expression of pERK1/2 was measured by Western blot.
RESULTS: The calvaria OBs treated with BSNXD serum showed more potent ability for cell proliferation than control groups (serum from the ovariectomized mice treated with saline). The BSNXD serum inhibited the etoposide-induced apoptosis of the OBs, with the effective concentrations of 10-20%. While being pretreated with the selective inhibitor of ERK1/2 U0126, the anti-apoptosis effect of the pharmacological serum on the OBs was almost completely blocked. Meanwhile, the expression of phosphor-pERK1/2 decreased significantly.
CONCLUSION: The BSNXD pharmacological serum promoted the proliferation and inhibited the apoptosis of the mouse OBs, which might be through the activation of MAPK signal transduction pathways and ERK1/2 activation via phosphoration of ERK.
METHODS: The ovariectomized BALB/c mice serving as a postmenopausal osteoporosis model were treated with BSNXD for 12 weeks. The serum from the mice was collected and applied to the cultivation of the calvaria OBs of newborn BALB/c litters. Cell proliferation was measured by methyl thiazolyl tetrazolium (MTT) assay. Apoptosis rate was analyzed by Annexin V-FITC/PI flow cytometry (FCM) and the expression of pERK1/2 was measured by Western blot.
RESULTS: The calvaria OBs treated with BSNXD serum showed more potent ability for cell proliferation than control groups (serum from the ovariectomized mice treated with saline). The BSNXD serum inhibited the etoposide-induced apoptosis of the OBs, with the effective concentrations of 10-20%. While being pretreated with the selective inhibitor of ERK1/2 U0126, the anti-apoptosis effect of the pharmacological serum on the OBs was almost completely blocked. Meanwhile, the expression of phosphor-pERK1/2 decreased significantly.
CONCLUSION: The BSNXD pharmacological serum promoted the proliferation and inhibited the apoptosis of the mouse OBs, which might be through the activation of MAPK signal transduction pathways and ERK1/2 activation via phosphoration of ERK.