Alleviation of diabetic nephropathy by zinc oxide nanoparticles in streptozotocin‐induced type 1 diabetes in rats

Abstract This study examines the effect of nanoparticles with zinc oxides (ZnONPs) on diabetic nephropathy, which is the primary cause of mortality for diabetic patients with end‐stage renal disease. Diabetes in adult male rats was induced via intraperitoneal injection of streptozotocin. ZnONPs were intraperitoneally administered to diabetic rats daily for 7 weeks. Diabetes was associated with increases in blood glucose level, 24‐h urinary albumin excretion rate, glomerular basement membrane thickness, renal oxidative stress markers, and renal mRNA or protein expression of transforming growth factor‐β1, fibronectin, collagen‐IV, tumour necrosis factor‐α and vascular endothelial growth factor‐A. Moreover, the expression of nephrin and podocin, and the mRNA expression of matrix metalloproteinase‐9 were decreased in the diabetic group. These changes were not detected in the control group and were significantly prevented by ZnONP treatment. These results provide evidence that ZnONPs ameliorate the renal damage induced in a diabetic rat model of nephropathy through improving renal functionality; inhibiting renal fibrosis, oxidative stress, inflammation and abnormal angiogenesis; and delaying the development of podocyte injury. The present findings may help design the clinical application of ZnONPs for protection against the development of diabetic nephropathy

Crocin treatment improves testosterone induced benign prostatic hyperplasia in rats

Background and objective: Benign prostatic hyperplasia (BPH) is a typical nonmalignant growth of the prostate in the elderly. Crocin, a bioactive component of Crocus sativus L., commonly known as saffron, is known to have an anti-proliferative activity against numerous types of cancer, including prostate cancer. This study investigated the effects of crocin on testosterone-induced BPH development in rats. Materials and methods: The study sample included three groups of adult male rats (3 months old, weighed 250 g): the control group received corn oil only, the second and the third groups were injected with testosterone (3 mg/kg dissolved in corn oil) subcutaneously. The second group was considered as testosterone-induced BPH (untreated) while the third groups were assigned as testosterone-induced BPH-crocin treated group (100 mg/kg orally for 14 days). Results: After animal sacrifice, histopathological analysis of the prostate tissues was performed in parallel with gene expression of proliferation (PCNA), inflammation (IL-6), and vascularization (VEGF-A) markers, analyzed by qRT-PCR. Crocin treatment significantly reduced prostate index and the thickness of the epithelial layer in rats with BPH. Additionally, the mRNA expression levels of PCNA, a marker of cell proliferation; IL-6, an inflammatory cytokine; and VEGF-A, an angiogenesis marker, were significantly down-regulated in the BPH group that were treated with crocin. Conclusions: The present study indicates that crocin can effectively prevent the development of experimentally induced BPH through inhibition of prostatic cellular proliferation, inflammation, and angiogenesis

Estimates of possible severe bacterial infection in neonates in sub-Saharan Africa, south Asia, and Latin America for 2012: A systematic review and meta-analysis

Background: Bacterial infections are a leading cause of the 2·9 million annual neonatal deaths. Treatment is usually based on clinical diagnosis of possible severe bacterial infection (pSBI). To guide programme planning, we have undertaken the first estimates of neonatal pSBI, by sex and by region, for sub-Saharan Africa, south Asia, and Latin America. Methods: We included data for pSBI incidence in neonates of 32 weeks' gestation or more (or birthweight ≥1500 g) with livebirth denominator data, undertaking a systematic review and forming an investigator group to obtain unpublished data. We calculated pooled risk estimates for neonatal pSBI and case fatality risk, by sex and by region. We then applied these risk estimates to estimates of livebirths in sub-Saharan Africa, south Asia, and Latin America to estimate cases and associated deaths in 2012. Findings: We included data from 22 studies, for 259 944 neonates and 20 196 pSBI cases, with most of the data (18 of the 22 studies) coming from the investigator group. The pooled estimate of pSBI incidence risk was 7·6% (95% CI 6·1-9·2%) and the case-fatality risk associated with pSBI was 9·8% (7·4-12·2). We estimated that in 2012 there were 6·9 million cases (uncertainty range 5·5 million-8·3 million) of pSBI in neonates needing treatment: 3·5 million (2·8 million-4·2 million) in south Asia, 2·6 million (2·1 million-3·1 million) in sub-Saharan Africa, and 0·8 million (0·7 million-1·0 million) in Latin America. The risk of pSBI was greater in boys (risk ratio 1·12, 95% CI 1·06-1·18) than girls. We estimated that there were 0·68 million (0·46 million-0·92 million) neonatal deaths associated with pSBI in 2012. Interpretation: The need-to-treat population for pSBI in these three regions is high, with ten cases of pSBI diagnosed for each associated neonatal death. Deaths and disability can be reduced through improved prevention, detection, and case management. Funding: The Wellcome Trust and the Bill and Melinda Gates Foundation through grants to Child Health Epidemiology Reference Group (CHERG) and Save the Children's Saving Newborn Lives programme. © 2014 Seale et al