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The prevalence of chronic kidney disease in diabetics is progressively increasing with an increased risk of fatal complications.Sixty male albino rats were used in the study, and type 2 diabetes mellitus were induced. Diabetic rats were divided randomly into 5 groups, the control diabetic group and 4 treated groups were treated with metformin (group3), dulaglutide (group 4), metformincilostazol (group 5), and the last group was treated with dulaglutidecilostazol (group 6). At the end of the experiment, the weight of rats and systolic blood pressure were estimated. After overnight fasting, the serum levels of blood glucose, lipid profile, and kidney function were measured. After scarification, gene expression of eNOS and NFKB in kidney tissue were estimated and kidney tissues were examined for histopathology.Diabetic rats showed a significant increase in body weight, blood pressure, serum blood glucose, lipid profile, and impaired kidney function. Metformin and dulaglutide are associated with a significant decrease in blood pressure, blood glucose level, serum lipid profile, and improved kidney function. These changes are associated with a significant increase in anti-oxidative markers, and decreased inflammatory and fibrotic markers, especially with the addition of cilostazol.Metformin and dulaglutide have been shown to ameliorate kidney damage in diabetics by stimulating the anti-oxidant defense system, normalizing kidney functional parameters, and improving histopathological changes. The addition of cilostazol to metformin or dulaglutide increased some of their anti-oxidants and anti-inflammatory properties.

Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease. We aimed to measure the level of miR-155 and its genetic variant rs767649 in patients with RA and to evaluate their rela...

Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease. We aimed to measure the level of miR-155 and its genetic variant rs767649 in patients with RA and to evaluate their relationship with ischemia-modified albumin (IMA). The study was performed on 79 patients with RA (group I) and 78 healthy control participants (group II). Quantitative real-time polymerase chain reaction was used to assess the expression of serum miR-155 in addition to its functional variant rs767649. IMA levels were measured by enzyme-linked immunosorbent assay. Significant overexpression of miR-155 and higher levels of IMA were detected in patients with RA compared with those in controls (

The effects of epigallocatechin-3-gallate (EGCG) and metformin single treatment have been tested against hepatocellular carcinoma (HCC). This study aimed to assess the combination effects of EGCG and metformin on proliferation and apoptosis of HepG2cells and identified new potential molecular targets. The effect of EGCG and metformin against cell proliferation in HepG2 was determined using MTT assay. Reverse transcription polymerase chain reaction was applied to examine the gene expression of cyclin D1, lncRNA-AF085935, caspase-3, survivin and VEGF. The level of protein expression of glypican-3 was assessed by western blot. In HepG2 cells, EGCG and metformin combination treatment exhibited high significant effect against tumor proliferation. It significantly reduced cyclin D1, lncRNA-AF085935, glypican-3 and promoted apoptosis through increasing caspase3 and decreasing survivin compared to control cells. Moreover, EGCG and metformin treated cells showed decreased expression levels of VEGF. Our study provided new insights of the anticarcinogenic effects of EGCG and metformin on HCC through their effects on glypican-3 and lncRNA-AF085935.

Background: Atherosclerosis is a complex disease of the arteries characterized by endothelial dysfunction, vascular inflammation, and the build-up of lipids within the intima of the vessel wall. Testosterone has a central or permissive role in pathogenesis of the metabolic syndrome and type 2 diabetes. Insulin resistance is associated with several CVD risk factors such as obesity, dyslipidaemia, hypertension and the proinflammatory state. We aim to disclose the relationship between serum testosterone concentration and carotid atherosclerosis and its risk factors in men with type 2 diabetes. Patients and methods: The study population comprised 123 consecutive men of Type 2 diabetes. Retinopathy and nephropathy were ranked and graded respectively. Cardiovascular disease was defined as the presence of previous myocardial infarction or cerebral infarction. Total cholesterol and triglyceride concentrations were determined and hemoglobin Alc was measured. Assessment for the presence of carotid atherosclerosis was done, using ultrasonographic measurement of carotid intima media thickness (IMT). The relationship between serum testosterone concentration and carotid intima-media thickness IMT was investigated in all patients. Results: The mean of IMT for all patients was 0.96 ± 0.28 mm. Mean IMT was significantly greater in patients with lower concentrations of F-tes than in patients with higher concentrations of F-tes. (P= 0.038). Relationship between serum free testosterone concentration and other variables showed a negative correlation with patients’ age, patients’ age at onset, duration of diabetes, BMI, HbA1c, systolic and diastolic blood pressure, and total cholesterol concentrations and mean IMT in men with type 2 diabetes. No significant correlation was found between F-tes with triglyceride and negative correlation with mean IMT. Conclusion: Serum free testosterone concentration was found to be low in type 2 diabetic men. It has a negative correlation with patients’ age, patients’ age at onset of the disease, duration of diabetes, BMI and HbA1c, total cholesterol concentrations systolic and diastolic blood pressure and mean IMT. This may disclose the different mechanisms played by testosterone in the pathogenesis of cardiovascular risk in men with type 2 diabetes.