Animal experiment:

Mice[2]8-12 weeks old C57/BL6 male mice between 23-25 g receive intraperitoneal (i.p.) injections of 50 mg/kg Streptozotocin (STZ), dissolved in 100 mM citrate buffer pH 4.5, for five consecutive days. Diabetic mice (13-week-old) are randomly divided into three groups: 1) untreated group; 2) Nedocromil group, with Nedocromil released at the rate of 30 mg/kg per day from a subcutaneous (s.c.) pellet implantation; and vehicle group, with an inactive pellet implanted. Normal mice (non-diabetic) and normal mice that receive Nedocromil (30 mg/kg per day) are also included in this study for comparison. All sample groups included 15 mice (n=15)[2].

Nedocromil sodium suppresses the action or formation of multiple mediators, including histamine, leukotriene C4 (LTC4), and prostaglandin D2 (PGD2).

Nedocromil inhibits the release of histamine, LTC4, and PGD2 from mast cells challenged with antigen (with IC30 values of 2.1 μM, 2.3 μM, and 1.9 μM, respectively) and with anti-human IgE (IC30 values of 4.7 μM, 1.3 μM, and 1.3 μM, respectively)[1].

Nedocromil-treated diabetic mice show significantly improved heart function compared with controls. The contractility and relaxation forces show similar improvements. However, the cardiac function of Nedocromil-treated diabetic mice remains significantly impaired when compared with normal mice. Nedocromil can significantly improve cardiac function in mice with diabetic cardiomyopathy, but the treatment cannot restore normal function[2].

References:
[1]. Wells E, et al. Characterization of primate bronchoalveolar mast cells. II. Inhibition of histamine, LTC4, and PGD2 release from primate bronchoalveolar mast cells and a comparison with rat peritoneal mastcells. J Immunol. 1986 Dec 15;137(12):3941-5.
[2]. Myocardial remodeling in diabetic cardiomyopathy associated with cardiac mast cell activation. Huang ZG, et al. PLoS One. 2013;8(3):e60827.