Busulfan (BUS) is an anticancer agent with serious adverse effects on various body organs, including the lung and testis. Sitagliptin was proven to have antioxidant, anti-inflammatory, antifibrotic, and antiapoptotic effects. This study aims to evaluate whether sitagliptin, a DPP4I, ameliorates BUS-induced pulmonary and testicular injury in rats. Male Wistar rats were split into control, sitagliptin (10 mg/kg), BUS (30 mg/kg), and sitagliptin + BUS groups. Weight change, lung and testis indices, serum testosterone, sperm parameters, markers of oxidative stress [malondialdehyde (MDA) and reduced glutathione (GSH)], inflammation [tumor necrosis factor-alpha (TNF-α)], and relative expression of sirtuin1 (SIRT1) and forkhead box protein type O1 (FOXO1) genes were estimated. Histopathological examination of lung and testicular tissues was done to detect architectural changes [Hematoxylin & Eosin (H&E)], fibrosis (Masson’s trichrome), and apoptosis (caspase-3). Sitagliptin treatment reduced body weight loss, lung index, lung and testis MDA, serum TNF-α and sperm abnormal morphology, and increased testis index, lung and testis GSH, serum testosterone, sperm count, viability and motility. SIRT1/FOXO1 balance was restored. Also, sitagliptin attenuated fibrosis and apoptosis in lung and testicular tissues via reducing collagen deposition and caspase-3 expression. Accordingly, sitagliptin ameliorated BUS-induced pulmonary and testicular damage in rats via attenuating oxidative stress, inflammation, fibrosis, and apoptosis.

Breast cancer is a major health threat to women globally. Many circulating microRNAs are non-invasive cancer biomarkers. In this study, the expression of miR-29b and miR-31 was assessed in blood samples from 200 patients with breast cancer and wholesome volunteer women using quantitative reverse transcriptase PCR to evaluate their role in the disease. MiR-29b was significantly overexpressed in patients compared to controls. Multivariate regression analysis showed that it was an established risk factor for relapse and mortality. MiR-31 was significantly under-expressed in patients. It was an established risk factor for relapse and was strongly associated with mortality. For the prediction of relapse, miR-29b had a sensitivity of 81.25% and a specificity of 88.24% at a cutoff of > 30.09, while miR-31 had a sensitivity of 87.50% and a specificity of 79.41% at a cutoff of 0.12. The specificity was enhanced to 100% by combining the values of miR-29b and miR-31. In predicting mortality, miR-29b exhibited a sensitivity of 90% and a specificity of 97.5% at a cutoff of > 48.10. At a cutoff of 0.119, miR-31 exhibited a sensitivity of 87.50% and a specificity of 79.41%. High miR-29b expression and low miR-31 expression were linked with a low survival rate. MiR-29b and miR-31 could be useful markers for predicting breast cancer relapse and mortality.