Diabetes mellitus is a common metabolic disorder affecting different body organs; one of its serious complications is diabetic cardiomyopathy (DCM). Thus, finding more cardiopreserving agents to protect the heart against such illness is a critical task. For the first time, we planned to study the suspected role of diacerein (DIA) in ameliorating DCM in juvenile rats and explore different mechanisms mediating its effect including inflammasome/caspase1/interleukin1β pathway. Four-week-aged juvenile rats were randomly divided into groups; the control group, diacerein group, diabetic group, and diabetic-treated group. Streptozotocin (45 mg/kg) single intraperitoneal (i.p.) dose was administered for induction of type 1 diabetes on the 1st day which was confirmed by detecting blood glucose level. DIA was given in a dose of 50 mg/kg/day for 6 weeks to diabetic and non-diabetic rats, then we evaluated different inflammatory, apoptotic, and oxidative stress parameters. Induction of DCM succeeded as there were significant increases in cardiac enzymes, heart weights, fasting blood glucose level (FBG), and glycosylated hemoglobin (HbA1c) associated with elevated blood pressure (BP), histopathological changes, and increased caspase 3 immunoexpression. Furthermore, there was an increase of malondialdehyde (MDA), inflammasome, caspase1, angiotensin II, nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNFα), and interleukin 1β (IL1β). However, antioxidant parameters such as reduced glutathione (GSH) and total antioxidant capacity (TAC) significantly declined. Fortunately, DIA reversed the diabetic cardiomyopathy changes mostly due to the observed anti-inflammatory, antioxidant, and anti-apoptotic properties with regulation of blood glucose level.DIA has an ability to regulate DCM-associated biochemical and histopathological disturbances.

Type 2 diabetes mellitus (T2DM) is a chronic global disease characterized by serious complications. Evidence has shown that free radicals’ formation is involved in the pathogenesis of the disease and development of its complications. T2DM is associated with disrupted glucose and lipid homeostasis with abnormal insulin sensitivity and/or secretion. No single treatment regimen is absolutely 100% effective. Metformin is a first-line treatment for T2DM whose main actions are the suppression of gluconeogenesis and the improvement of glucose uptake and insulin sensitivity. However, the exact mechanism of action is not clearly understood. Purpose of the study; Therefor, the current study aimed to assess the protective effects of metformin against diabetic complications in rats with explanation of the possible underlying mechanisms. Basic procedures; rats were allocated in 3 groups. group1: control (C) received normal pellet diet (NPD), group2: diabetic (D) received high fat diet (HFD) for 2 weeks then injected intra-peritoneally (IP) with single low dose of streptozotocin (STZ) (30 mg/kg), group3: diabetic metformin treated (DM) received metformin 500 mg/kg/day by gavage for 4 weeks. Rats were sacrificed after 4 weeks of treatment. Main findings: The damaging effect of STZ on the pancreatic beta cells resulted in T2DM that was evaluated by assessment of glucose, insulin, Homeostasis model assessment of insulin resistance (HOMA-IR), TGs, LDL, HDL, Urea, and malodialdehyde (MDA) in the diabetic rats ’serum. Principle conclusion: The results suggested the protective effects of metformin on ameliorating the diabetic effects.

Objective. Ovarian torsion is a gynecological emergency that occurs mostly during the female reproductive years due to ovarian masses or surgical manipulation. This work aims to explore the probable protective effect of leptin on rat ovaries due to ischemia-reperfusion (IR) injury. Methods. Wistar albino rats were divided into four groups: 1) control group; 2) ovarian IR group (OVIR); 3) leptin group I [OVIR + leptin (10 µg/kg body weight, b.w.)]; and 4) leptin group II (OVIR + leptin (100 µg/kg b.w.)]. Serum levels of estradiol and anti-Mullerian hormone (AMH) were measured. Levels of oxidative stress and inflammatory markers in ovarian tissue were determined along with the expression of sirtuin 1 (Sirt1), nuclear erythroid factor-2 (Nrf2), cyclooxygenase-2 (COX-2), nuclear factor kappa (NF-κB), toll like receptor-4 (TLR4), and caspase-3. Results. Serum estradiol and AMH levels were decreased with increased expression of COX-2, TLR4, caspase-3, and NF-κB and decreased expression of Sirt1and Nrf2 in ovary of the OVIR group, which were improved by exogenous administration of both leptin doses. Conclusion. Leptin administration dose-dependently reduced the severity of OVIR injury via modulation of Sirt-1/Nrf2 and TLR4/NF-kB/caspase-3 signaling pathways. Thus, leptin may be used as an adjuvant measure to prevent ovarian damage and improve the outcomes. However, clinical studies are needed to evaluate these results in humans.