Li Ling, Zhang Yong-Gang, Tan Yu-Fei, Zhao Jing-Jing, Zhang Hua-Ru, Zhao Bing
Department of Respiratory and Critical Care, Zhumadian Central Hospital, Zhumadian, Henan 463000, P.R. China.
Oncol Lett. 2018 Feb;15(2):2550-2554. doi: 10.3892/ol.2017.7581. Epub 2017 Dec 11.
The present study aimed to investigate the effect of tanshinone II, isolated from Bunge, on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats. Male Sprague-Dawley rats were divided into three groups: Control, LPS and tanshinone II. Animals in the tanshinone II and LPS groups were administered 10 mg/kg LPS, whereas those in the control group received an equal volume of normal saline. Tanshinone II treatment group were injected with 30 nm/kg tanshinone II at 1 h after LPS administration. The results revealed that LPS administration increased the bronchoalveolar lavage fluid protein concentration significantly compared with the control group. However, tanshinone II treatment significantly inhibited the LPS-induced increase in protein level. Treatment of the LPS-administered rats with tanshinone II prevented the formation of pulmonary edema, which was evidenced by low values for wet to dry lung weight ratio. The activity of myeloperoxidase and expression of malondialdehyde were significantly lower in lung homogenates from the tanshinone II group compared with the LPS group. Furthermore, tanshinone II treatment inhibited the expression of tumor necrosis factor-α and interleukin-6 in the blood plasma. Tissue sections of the tanshinone II group exhibited normal morphology and absence of neutrophil accumulation. However, in the LPS group, neutrophils accumulated and penetrated into the pulmonary tissues. These results suggested that tanshinone II protects the rats from LPS-induced ALI. Therefore tanshinone II may have clinical applications in the treatment of ALI.
本研究旨在探讨从丹参中分离得到的丹参酮II对脂多糖(LPS)诱导的大鼠急性肺损伤(ALI)的影响。雄性Sprague-Dawley大鼠分为三组:对照组、LPS组和丹参酮II组。丹参酮II组和LPS组的动物给予10 mg/kg LPS,而对照组的动物给予等量的生理盐水。丹参酮II治疗组在给予LPS后1小时注射30 mg/kg丹参酮II。结果显示,与对照组相比,给予LPS显著增加了支气管肺泡灌洗液蛋白浓度。然而,丹参酮II治疗显著抑制了LPS诱导的蛋白水平升高。用丹参酮II治疗给予LPS的大鼠可预防肺水肿的形成,肺湿重与干重比值较低证明了这一点。与LPS组相比,丹参酮II组肺匀浆中髓过氧化物酶活性和丙二醛表达显著降低。此外,丹参酮II治疗抑制了血浆中肿瘤坏死因子-α和白细胞介素-6的表达。丹参酮II组的组织切片显示形态正常且无中性粒细胞积聚。然而,在LPS组中,中性粒细胞积聚并渗入肺组织。这些结果表明,丹参酮II可保护大鼠免受LPS诱导的ALI。因此,丹参酮II可能在ALI的治疗中具有临床应用价值。