Chen Lianghua, Ma Qiujuan, Zhang Gongye, Lei Yongbin, Wang Weiwei, Zhang Yuqi, Li Tingting, Zhong Wei, Ming Yanlin, Song Gang
Key Laboratory of Fujian Province for physiology and Biochemistry of Subtropical Plant, Fujian Institute of Subtropical Botany, Xiamen, Fujian 361006, China.
Cancer Research Center, School of Medicine, Xiamen University, Xiamen 361102, China.
Phytomedicine. 2022 May;99:154030. doi: 10.1016/j.phymed.2022.154030. Epub 2022 Mar 5.
Loganin and morroniside are two iridoid glycosides with anti-inflammatory, antioxidant and anti-tumor effects. Whether they have effect on acute lung injury and pulmonary fibrosis are still unknown.
To explore the potential effects of loganin and morroniside against acute lung cancer and pulmonary fibrosis, and the underlying molecular mechanism.
Cell and animal models of acute lung injury were established by the induction of LPS. After intervention with loganin and morroniside, the pathological symptom of lung tissue was assessed, pro-inflammatory factors in cells and lung tissues were detected, NF- κB/STAT3 signaling pathway related proteins were detected by western blotting. Mice pulmonary fibrosis model was induced by bleomycin, pathological symptom was assessed by HE and Masson staining. Fibrosis related indicators were detected by qPCR or western blot. CD4+/CD8+ was detected by flow cytometry.
Loganin and morroniside relieved the pathological symptom of lung tissue in acute lung injury, pro-inflammatory factors such as IL-6, IL-1β, TNF-α mRNA were inhibited. Expression of p-p65 and STAT3 in lung tissues were also downregulated. In addition, loganin and morroniside downregulated the expression of collagen fiber, hydroxyproline and TGF-β1, collagen I and α-SMA mRNA in lung tissues of pulmonary fibrosis model. This study proved that loganin and morroniside have protective effect on acute lung injury and pulmonary fibrosis, and may provide theoretical basis for the development of new clinical drugs.
马钱苷和莫诺苷是两种具有抗炎、抗氧化和抗肿瘤作用的环烯醚萜苷。它们对急性肺损伤和肺纤维化是否有作用仍不清楚。
探讨马钱苷和莫诺苷对急性肺损伤和肺纤维化的潜在作用及其潜在分子机制。
通过脂多糖诱导建立急性肺损伤的细胞和动物模型。用马钱苷和莫诺苷干预后,评估肺组织的病理症状,检测细胞和肺组织中的促炎因子,通过蛋白质印迹法检测NF-κB/STAT3信号通路相关蛋白。用博来霉素诱导小鼠肺纤维化模型,通过苏木精-伊红染色和Masson染色评估病理症状。通过定量聚合酶链反应或蛋白质印迹法检测纤维化相关指标。通过流式细胞术检测CD4+/CD8+。
马钱苷和莫诺苷减轻了急性肺损伤中肺组织的病理症状,抑制了白细胞介素-6、白细胞介素-1β、肿瘤坏死因子-α等促炎因子的信使核糖核酸。肺组织中p-p65和信号转导和转录激活因子3的表达也下调。此外,马钱苷和莫诺苷下调了肺纤维化模型肺组织中胶原纤维、羟脯氨酸和转化生长因子-β1、I型胶原和α-平滑肌肌动蛋白信使核糖核酸的表达。本研究证明马钱苷和莫诺苷对急性肺损伤和肺纤维化具有保护作用,可能为开发新的临床药物提供理论依据。