PDF(Pubmed)
Abstract：
UNASSIGNED: In recent years, the incidence of chronic obstructive pulmonary disease (COPD) has been increasing year by year, but therapeutic drugs has no breakthrough. The total alkaloid extract from Bulbus Fritillariae pallidiflorae (BFP-TA) is widely used in treating lung diseases. Therefore, this study aimed to investigate the protective effect and mechanism of BFP-TA in COPD mice.
UNASSIGNED: BFP-TA was prepared by macroporous adsorbent resin, and the material basis of BFP-TA was analyzed by HPLC-ELSD and UHPLC-MS/MS. Then, the COPD mouse model was induced by cigarette smoke (CS) for 12 weeks, administered at weeks 9-12. Subsequently, the body weight, lung-body ratio, pulmonary function, histopathology, and the levels of pro-inflammatory cytokines, matrix metalloproteinases (MMPs) and oxidative stress markers in the serum of mice were determined. The expressions of related protein of EMT and MAPK signaling pathways in the lung tissues of mice were detected by Western blot.
UNASSIGNED: The alkaloid relative content of BFP-TA is 64.28%, and nine alkaloids in BFP-TA were identified and quantified by UHPLC-MS/MS. Subsequently, the animal experiment showed that BFP-TA could improve pulmonary function, and alleviate inflammatory cell infiltration, pulmonary emphysema, and collagen fiber deposition in the lung of COPD mice. Furthermore, BFP-TA could decrease the levels of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β), MMPs (MMP-9 and MMP-12) and MDA, while increase the levels of TIMP-1 and SOD. Moreover, BFP-TA could decrease the protein expressions of collagen I, vimentin, α-SMA, MMP-9, MMP-9/TIMP-1, Bax, p-JNK/JNK, p-P38/P38, and p-ERK/ERK, while increase the level of E-cadherin.
UNASSIGNED: This study is the first to demonstrate the protective effect of BFP-TA in CS-induced COPD mouse model. Furthermore, BFP-TA may improve airway remodeling by inhibiting the EMT process and potentially exert anti-inflammatory effect by inhibiting the MAPK signaling pathway.
UNASSIGNED: BFP-TA was prepared by macroporous adsorbent resin, and the material basis of BFP-TA was analyzed by HPLC-ELSD and UHPLC-MS/MS. Then, the COPD mouse model was induced by cigarette smoke (CS) for 12 weeks, administered at weeks 9-12. Subsequently, the body weight, lung-body ratio, pulmonary function, histopathology, and the levels of pro-inflammatory cytokines, matrix metalloproteinases (MMPs) and oxidative stress markers in the serum of mice were determined. The expressions of related protein of EMT and MAPK signaling pathways in the lung tissues of mice were detected by Western blot.
UNASSIGNED: The alkaloid relative content of BFP-TA is 64.28%, and nine alkaloids in BFP-TA were identified and quantified by UHPLC-MS/MS. Subsequently, the animal experiment showed that BFP-TA could improve pulmonary function, and alleviate inflammatory cell infiltration, pulmonary emphysema, and collagen fiber deposition in the lung of COPD mice. Furthermore, BFP-TA could decrease the levels of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β), MMPs (MMP-9 and MMP-12) and MDA, while increase the levels of TIMP-1 and SOD. Moreover, BFP-TA could decrease the protein expressions of collagen I, vimentin, α-SMA, MMP-9, MMP-9/TIMP-1, Bax, p-JNK/JNK, p-P38/P38, and p-ERK/ERK, while increase the level of E-cadherin.
UNASSIGNED: This study is the first to demonstrate the protective effect of BFP-TA in CS-induced COPD mouse model. Furthermore, BFP-TA may improve airway remodeling by inhibiting the EMT process and potentially exert anti-inflammatory effect by inhibiting the MAPK signaling pathway.
摘要：
■近年来，慢性阻塞性肺疾病(COPD)的发病率逐年上升,但是治疗药物没有突破。白贝母总生物碱提取物(BFP-TA)广泛应用于肺部疾病的治疗。因此,本研究旨在探讨BFP-TA对COPD小鼠的保护作用及其机制。
■采用大孔吸附树脂制备BFP-TA,通过HPLC-ELSD和UHPLC-MS/MS分析BFP-TA的物质基础。然后，用香烟烟雾(CS)诱导COPD小鼠模型12周,在第9-12周施用。随后，体重,肺体比，肺功能,组织病理学,和促炎细胞因子的水平，测定小鼠血清中的基质金属蛋白酶(MMPs)和氧化应激标志物。Westernblot检测小鼠肺组织中EMT相关蛋白和MAPK信号通路的表达。
■BFP-TA的生物碱相对含量为64.28%,通过UHPLC-MS/MS鉴定和定量BFP-TA中的9种生物碱。随后，动物实验表明BFP-TA能改善肺功能,减轻炎症细胞浸润，肺气肿,COPD小鼠肺内胶原纤维沉积。此外，BFP-TA可以降低促炎细胞因子（TNF-α，IL-6和IL-1β），MMPs（MMP-9和MMP-12）和MDA，同时增加TIMP-1和SOD的水平。此外，BFP-TA可以降低I型胶原的蛋白表达,波形蛋白,α-SMA,MMP-9，MMP-9/TIMP-1，Bax，p-JNK/JNK,p-P38/P38和p-ERK/ERK,同时增加E-cadherin的水平。
■这项研究首次证明了BFP-TA在CS诱导的COPD小鼠模型中的保护作用。此外，BFP-TA可能通过抑制EMT过程改善气道重塑，并可能通过抑制MAPK信号通路发挥抗炎作用。
■采用大孔吸附树脂制备BFP-TA,通过HPLC-ELSD和UHPLC-MS/MS分析BFP-TA的物质基础。然后，用香烟烟雾(CS)诱导COPD小鼠模型12周,在第9-12周施用。随后，体重,肺体比，肺功能,组织病理学,和促炎细胞因子的水平，测定小鼠血清中的基质金属蛋白酶(MMPs)和氧化应激标志物。Westernblot检测小鼠肺组织中EMT相关蛋白和MAPK信号通路的表达。
■BFP-TA的生物碱相对含量为64.28%,通过UHPLC-MS/MS鉴定和定量BFP-TA中的9种生物碱。随后，动物实验表明BFP-TA能改善肺功能,减轻炎症细胞浸润，肺气肿,COPD小鼠肺内胶原纤维沉积。此外，BFP-TA可以降低促炎细胞因子（TNF-α，IL-6和IL-1β），MMPs（MMP-9和MMP-12）和MDA，同时增加TIMP-1和SOD的水平。此外，BFP-TA可以降低I型胶原的蛋白表达,波形蛋白,α-SMA,MMP-9，MMP-9/TIMP-1，Bax，p-JNK/JNK,p-P38/P38和p-ERK/ERK,同时增加E-cadherin的水平。
■这项研究首次证明了BFP-TA在CS诱导的COPD小鼠模型中的保护作用。此外，BFP-TA可能通过抑制EMT过程改善气道重塑，并可能通过抑制MAPK信号通路发挥抗炎作用。
