Tanshinone IIA attenuates ovalbumin-induced airway inflammation and hyperresponsiveness in a murine model of asthma

Iran J Basic Med Sci. 2019 Feb;22(2):160-165. doi: 10.22038/ijbms.2018.30598.7375.

Abstract

Objectives: Tanshinone IIA (T. IIA), one of the most pharmacologically active components extracted from Salviae miltiorrhiza, has anti-inflammatory and antioxidant features. The aim of the present study is to investigate the benefit of T. IIA on asthma using a murine model of asthma induced by ovalbumin (OVA).

Materials and methods: Male BALB/c mice were used in the present study. The mice were sensitized by OVA intraperitoneal injection on days 0 and 14, and received aerosolized OVA challenge for 30 min daily on days 21-23. T. IIA (10 mg/kg twice daily) intraperitoneal injection was performed on days 18-23.

Results: Treatment of T. IIA reduced the levels of interleukin (IL)-4, IL-5, and IL-13 in bronchoalveolar lavage fluid (BALF) (P<0.05 for all cases). The OVA-induced elevation of total white blood cells as well as differential white blood cells in BALF and blood were inhibited by T. IIA (P<0.05 for all cases). Moreover, airway hyperresponsiveness was dampened in T. IIA-treated group (P<0.05). T. IIA inhibited the activation of nuclear factor-κB in asthmatic mice (P<0.05). The activity of nuclear factor erythroid-2-related factor 2 was enhanced in T. IIA-treated group (P<0.05). T. IIA elevated the activities of heme oxygenase-1, glutathione peroxidase, and superoxide dismutase (P<0.05 for all cases).

Conclusion: T. IIA inhibits OVA-induced airway inflammation and hyperresponsiveness. T. IIA is a potential therapeutic agent for asthma.

Keywords: Asthma; Inflammation; Nuclear factor-κB; Oxidative stress; Tanshinone IIA.