Protective effects of co-administration of gallic Acid and cyclosporine on rat myocardial morphology against ischemia/reperfusion

Abstract

Background: Irreversible myocardial ischemic injury begins 20 minutes after the onset of coronary occlusion. Then the infarcted cells show signs of necrosis and death.

Objectives: This study investigated the effects of co-administration of Gallic acid (antioxidant) with cyclosporine (mitochondrial permeability transition pore [mPTP] inhibitor) on myocardial morphology of rats during ischemia and reperfusion.

Materials and methods: Fifty-four male Wistar rats (250-300 g), were randomly divided into 9 groups: sham, control (Ca received saline, 1 mL/kg, Cb: perfused with cyclosporine CsA 0.2 µM), 3 groups pretreated with Gallic acid in saline (G1a:7.5, G2a:15, and G3a: 30 mg/kg/day, and gavage daily for 10 days, n = 6), and the other three groups were pretreated with Gallic acid then perfused using CsA, (G1b:7.5, G2b:15, and G3b: 30 mg/kg/day) at the first 13 minutes of reperfusion period. After 10 days pretreatment, the rat hearts were isolated and transferred to Langendorff apparatus and exposed to 30 minutes ischemia following 60 minutes reperfusion. Afterward, the hearts were preserved in 10% formalin for histological studies at the end of the experiment. Finally, hematoxylin and eosin and Masson's trichrome staining techniques were used for evaluating the changes in myocardial architecture, degradation of myofibers, and collagen integrity. The differences were analyzed using Pearson test.

Results: Cell degenerative changes, pyknotic nuclei, contraction bands, edema, and loosening of collagen in between muscle fibers were observed during ischemia-reperfusion. Myocardial architecture and cellular morphology were recovered in co-administration groups, especially in (Gallic acid 15 mg/kg + CsA, P < 0.001).

Conclusions: The results suggest the important role of the antioxidant system potentiation in the prevention of myocardial damage.

Keywords: Collagens; Heart; Mitochondria; Oxidative Stress.

Figure 1.. Hematoxylin and Eosin Histological Stained of the Myocardial Tissue (×400)

Edema (ED), pyknotic nuclei (PKN), contraction bands (CB), necrosis (N), wavy fibers (W). Sham: a group that did not expose to ischemia. A, control group received saline; B, group received CsA; C, group received Gallic acid (7.5 mg/kg); D, group received Gallic acid (7.5 mg/kg + CsA); E, group received Gallic acid (15 mg/kg); F, group received Gallic acid (15 mg/kg + CsA); G, group received Gallic acid (30 mg/kg); H, group received Gallic acid (30 mg/kg + CsA).

Figure 2.. Masson’s Trichrome Histological Stained of Myocardial Tissues (× 400)

Sham: a group that did not expose to ischemia, A, Control group received saline; B, group received CsA; C, group received Gallic acid (7.5 mg/kg); D, group received Gallic acid (7.5 mg/kg + CsA); E, group received Gallic acid (15 mg/kg); F, group received Gallic acid (15 mg/kg + CsA); G, group received Gallic acid (30 mg/kg); H, group received Gallic acid (30 mg/kg + CsA).