BACKGROUND We studied the protective effects of Qingyi decoction(QYD)(a Traditional Chinese Medicine)against severe acute pancreatitis(SAP)-induced myocardial infarction(MI).AIM To study the function and mechanism of ...BACKGROUND We studied the protective effects of Qingyi decoction(QYD)(a Traditional Chinese Medicine)against severe acute pancreatitis(SAP)-induced myocardial infarction(MI).AIM To study the function and mechanism of QYD in the treatment of myocardial injuries induced by SAP.METHODS Ultrasonic cardiography,hematoxylin and eosin staining,immunohistochemistry,qRT-PCR,western blot,enzyme-linked immunosorbent assays,and apoptosis staining techniques were used to determine the effects of QYD following SAP-induced MI in Sprague-Dawley rats.RESULTS Our SAP model showed severe myocardial histological abnormalities and marked differences in the symptoms,mortality rate,and ultrasonic cardiography outputs among the different groups compared to the control.The expression of serum cytokines[interleukin(IL)-1?,IL-6,IL-8,IL-12,amyloidβ,and tumor necrosis factor-α]were significantly higher in the SAP versus QYD treated group(P<0.05 for all).STIM1 and Orai1 expression in myocardial tissue extracts were significantly decreased post QYD gavage(P<0.001).There was no significant histological difference between the 2-aminoethyl diphenylborinate inhibitor and QYD groups.The SAP group had a significantly higher apoptosis index score compared to the QYD group(P<0.001).CONCLUSION QYD conferred cardio-protection against SAP-induced MI by regulating myocardial-associated protein expression(STIM1 and Orai1).展开更多
Objective: To examine the role of store-operated calcium entry(SOCE) and stromal interaction molecule 1(STIM1) in survival and migration of osteosarcoma cells and investigate what blockade of store-operated Ca^(2+)con...Objective: To examine the role of store-operated calcium entry(SOCE) and stromal interaction molecule 1(STIM1) in survival and migration of osteosarcoma cells and investigate what blockade of store-operated Ca^(2+)contributes to the regulation of osteosarcoma cells.Methods: First, we examined the expression levels of STIM1 in osteosarcoma cell lines by Western analysis and in tissue specimens by immunohistochemistry. Second, we investigated the effect of SOCE and STIM1 on osteosarcoma cell viability using MTS assays and on cell proliferation using colony formation. Third, we investigated the role of SOCE and STIM1 in cell migration using wound healing assays and Boyden chamber assays. Finally, we studied the effect of SOCE on the nuclear factor of activated T-cells cytoplasmic 1(NFATc1)activity by luciferase assays.Results: STIM1 was overexpressed in osteosarcoma cell lines and tissue specimens and was associated with poor survival of osteosarcoma patients. Also, inhibition of SOCE and STIM1 decreased the cell viability and migration of osteosarcoma cells. Furthermore, our results showed that blockade of store-operated Ca^(2+) channels involved down-regulation of NFATc1 in osteosarcoma cells.Conclusions: STIM1 is essential for osteosarcoma cell functions, and STIM1 and Ca^(2+) entry pathway could be further explored as molecular targets in the treatment of osteosarcoma.展开更多
基金the National Natural Science Foundation of China,No,81573751.
文摘BACKGROUND We studied the protective effects of Qingyi decoction(QYD)(a Traditional Chinese Medicine)against severe acute pancreatitis(SAP)-induced myocardial infarction(MI).AIM To study the function and mechanism of QYD in the treatment of myocardial injuries induced by SAP.METHODS Ultrasonic cardiography,hematoxylin and eosin staining,immunohistochemistry,qRT-PCR,western blot,enzyme-linked immunosorbent assays,and apoptosis staining techniques were used to determine the effects of QYD following SAP-induced MI in Sprague-Dawley rats.RESULTS Our SAP model showed severe myocardial histological abnormalities and marked differences in the symptoms,mortality rate,and ultrasonic cardiography outputs among the different groups compared to the control.The expression of serum cytokines[interleukin(IL)-1?,IL-6,IL-8,IL-12,amyloidβ,and tumor necrosis factor-α]were significantly higher in the SAP versus QYD treated group(P<0.05 for all).STIM1 and Orai1 expression in myocardial tissue extracts were significantly decreased post QYD gavage(P<0.001).There was no significant histological difference between the 2-aminoethyl diphenylborinate inhibitor and QYD groups.The SAP group had a significantly higher apoptosis index score compared to the QYD group(P<0.001).CONCLUSION QYD conferred cardio-protection against SAP-induced MI by regulating myocardial-associated protein expression(STIM1 and Orai1).
基金supported by Mayo Clinic, USA and Peking University People’s Hospital, Beijing, China
文摘Objective: To examine the role of store-operated calcium entry(SOCE) and stromal interaction molecule 1(STIM1) in survival and migration of osteosarcoma cells and investigate what blockade of store-operated Ca^(2+)contributes to the regulation of osteosarcoma cells.Methods: First, we examined the expression levels of STIM1 in osteosarcoma cell lines by Western analysis and in tissue specimens by immunohistochemistry. Second, we investigated the effect of SOCE and STIM1 on osteosarcoma cell viability using MTS assays and on cell proliferation using colony formation. Third, we investigated the role of SOCE and STIM1 in cell migration using wound healing assays and Boyden chamber assays. Finally, we studied the effect of SOCE on the nuclear factor of activated T-cells cytoplasmic 1(NFATc1)activity by luciferase assays.Results: STIM1 was overexpressed in osteosarcoma cell lines and tissue specimens and was associated with poor survival of osteosarcoma patients. Also, inhibition of SOCE and STIM1 decreased the cell viability and migration of osteosarcoma cells. Furthermore, our results showed that blockade of store-operated Ca^(2+) channels involved down-regulation of NFATc1 in osteosarcoma cells.Conclusions: STIM1 is essential for osteosarcoma cell functions, and STIM1 and Ca^(2+) entry pathway could be further explored as molecular targets in the treatment of osteosarcoma.
