Aminoguanidine mitigates apoptosis, testicular seminiferous tubules damage, and oxidative stress in streptozotocin-induced diabetic rats

Amelioration effects of nanoencapsulated triterpenoids from petri dish-cultured <em>Antrodia cinnamomea</em> on reproductive function of diabetic male rats

“…Several studies reported that SOD, GPx, and CAT were decreased in diabetic rat model. 5,68,70,71 In the present study, the Nano-PAC5-treated STZ-induced diabetic rats inhibited the oxidative stress by increasing the antioxidant activities of SOD, GPx, and CAT.…”

“…68 In diabetic rats, seminiferous tubule diameter was found to be decreased; basement membrane was found to be thickened in seminiferous tubules, and the degenerated germ cell was also seen. 69 In addition, Orman et al 68 reported an Table 3 The testis, epididymis, and epididymal adipose weight (% of body weight) in sTZ-induced diabetic rats fed different doses of Nano-Pac after 42 days atrophy of the seminiferous tubules and a dissociation with tubular shedding of immature spermatogenic cells in the diabetic model. Oral supplementation of Nano-PAC5 had amelioration effects on tubular diameter by stimulating cell survival and spermatogenesis due to Nano-PAC5-mediated alleviation of oxidative stress.…”

“…Hyperglycemia is known to reduce the activity of SOD in the sciatic nerve of the animal, 5 increase glycolysis, activate the intracellular sorbitol (polyol) pathway, and increase free radical formation. 68 SOD protects biological tissues from highly reactive superoxide anions (O 2 -) by converting them to H 2 O 2 , whereas CAT plays a role in the catalytic decomposition of harmful H 2 O 2 to O 2 and H 2 O. In the absence of breakdown by CAT or GPx, Hydrogen peroxidase (H 2 O 2 ) lead to the production of reactive hydroxyl radicals, reduce the cellular protection and make tissues easier to attack by free radicals.…”

Dietary resistant maltodextrin ameliorates testicular function and spermatogenesis in streptozotocin-nicotinamide-induced diabetic rats

“…Some studies showed that the apoptotic cell death play an important role in STZ‐induced diabetic rat testicular damage, and the possible mechanisms could be due to STZ cytotoxicity and/or diabetes‐related spermatogenic dysfunction through the regulation of Wnt 4, NF‐κB, VEGF, NGF‐β, TGF‐β1, IL‐1β, caspase 3, etc. (Roy et al ., ; Sisman et al ., ; Xu et al ., ; Orman et al ., ). In this STZ–nicotinamide‐induced diabetic rat, our result showed that upregulation of Bax/Bcl‐2 and caspase 8 in the diabetic group indicating the possible involvement of intrinsic pathway and extrinsic pathway respectively.…”

Therapeutic effect of pentoxifylline on reproductive parameters in diabetic male mice

“…During progression of diabetes mellitus, altered metabolism of lipids, carbohydrates and proteins increase lipid peroxides and production of reactive oxygen species (ROS) that induce oxidative stress on tissues (Jakus, ; Scarano et al ., ; Khaki et al ., ). Moreover, there is a strong relation between oxidative stress and increasing amount of apoptosis in testicular tissue of diabetic rats (Orman et al ., ). Oxidative stress is recognised as an eminent mediator of mitochondrial apoptosis (Visser et al ., ; Rocha‐Santos et al ., ).…”