Figure 6.

Effect of aging, NLRP3 deletion, and melatonin supplementation on morphological architecture of cardiac muscle fibers. (a) Semithin left ventricle sections of young (Y) WT mice stained by toluidine blue stain showing normal cardiac muscle fiber (M) architecture, with centrally positioned nucleus (N), and narrow interstitial spaces (asterisk) containing blood capillaries (BC) and fibroblasts (F). Note the intercalated disc (white arrow). (b) Cardiomyocytes (M) of early-aged (EA) WT mice revealing conservation of their striations with widening of interstitial spaces (asterisk). (c) The preservative effect of melatonin on maintaining normal cardiac fiber (M) architecture in EA animals. Numerous fibroblasts (F) were shown. (d) Cardiac muscle fibers of old-aged (OA) WT mice demonstrating disorganization of cardiomyocytes (M), loss of striation, and splitting of the nucleus (black arrow). (e) The protective effect of melatonin on conserving cardiac muscle fiber (M) orientation and striation in OA animals. (f) Left ventricle of Y NLRP3^−/− mice showing normal organization of the cardiomyocytes (M). (g,i) Cardiac muscle fibers (M) of the EA and OA NLRP3^−/− mice, respectively, revealing no structural changes, except increased interstitial tissues (asterisks) and blood capillaries (BC) in OA muscles. (h,j) Depicts the preservative effect of melatonin on cardiomyocyte (M) architecture in EA and OA NLRP3^−/− mice, respectively, revealing normal orientation and striation with narrow interstitial space containing blood capillaries (BC). Bar = 10 µm.