ACE2/ACE imbalance mediates bisphenol A-induced lung injury in Wistar rats: Results from captopril versus losartan histo-biochemical study.

Bisphenol-A (BPA) is a synthetic chemical compound broadly used in the plastic and epoxy resin industries with a considerable potential for food contamination. Literary reports have suggested that the altered renin-angiotensin system (RAS) is a mechanism for lung injury and inflammation caused by variable agents. The current study sought to investigate the contribution of RAS to BPA-induced lung damage. Moreover, the study assessed whether angiotensin II and/or bradykinin pathways were involved. For this aim, the angiotensin-converting enzyme (ACE) inhibitor captopril (Cap), either alone or combined with bradykinin receptor antagonist icatibant (Icat), was attempted versus the angiotensin receptor blocker losartan (Los). An eight-week study was conducted on forty Wistar male albino rats randomly divided into five equal groups: control, BPA, BPA/Cap, BPA/Los, and BPA/Cap/Icat groups. Captopril (100 mg/mL) and losartan (200 mg/mL) were given orally in drinking water, but icatibant (Icat) was injected subcutaneously (250 µg/kg) during the last two weeks of captopril treatment. Biochemical analysis of bronchoalveolar lavage fluid (BALF) and lung tissues, polymerase chain reaction (PCR) assay for ACE, ACE2, and caspase-3 genes expression, and histological and immunohistochemical studies were carried out to evaluate BPA-mediated pulmonary inflammation/apoptosis. BPA impaired the histological structure of the lungs, increased ACE, ACE2, and caspase-3 expressions at both gene/protein levels, and increased BALF inflammatory cytokines and lung oxidative markers. Inhibiting the ACE activity by captopril maintained the histological lung injury score, restored inflammation and the ACE2/ACE balance, and decreased apoptosis. Further improvement was obtained by the angiotensin II receptor (ATR1) blocker losartan. Icatibant (bradykinin B2 receptor blocker) didn't counteract the observed captopril effects. It was strongly suggested that RAS contributed to BPA-induced lung damage via alteration of ACE2 and ACE expression mediating angiotensin II generation rather than bradykinin.

Predictive urinary RNA biomarkers of kidney injury after extracorporeal shock wave lithotripsy.

BACKGROUND: Extracorporeal shock wave lithotripsy (ESWL) is considered one of the best choices for the treatment of various kinds of urinary tract calculi, although it might cause acute kidney injury. OBJECTIVE: To measure the urinary long non-coding RNA-messenger RNA (LncRNA-mRNA) panel before and after ESWL to evaluate post-ESWL renal injury in a reliable and non-invasive method. PATIENTS AND METHODS: The study included 60 patients with renal stones treated with ESWL and 30 healthy volunteers. Voided urine samples were obtained before, 2 h, and 1 day after ESWL. We measured the urinary level of LncRNA (SBF2-AS1, FENDRR-19) and mRNA (GBP1, NLRP3) by real-time qPCR and compared the results with serum creatinine and eGFR. RESULTS: LncRNA (SBF2-AS1, FENDRR-19) and mRNA (GBP1, NLRP3) levels were higher in patients with renal stones when compared with healthy volunteers. They showed a statistically significant increase in the level of LncRNA-mRNA panel in baseline and after ESWL treatment. CONCLUSION: LncRNA (SBF2-AS1, FENDRR-19) and mRNA (GBP1, NLRP3) levels were significantly elevated following ESWL treatment, highlighting the usefulness of urinary biomarkers in identifying patients at higher risk of developing renal injury after ESWL treatment.

Decellularized liver bioscaffold: a histological and immunohistochemical comparison between normal, fibrotic and hepatocellular carcinoma.

AIM OF THE STUDY: Increasing demand for liver transplantation represents an important health burden. Decellularized liver bioscaffold can be a suitable alternative for whole organ transplantation. However, various pathologies can affect the structure of decellularized scaffolds.This work discusses differences between hepatic fibrosis (HF), hepatocellular carcinoma (HCC) and normal decellularized liver bioscaffolds. MATERIAL AND METHODS: Murine models of HF and HCC were created, livers from normal, HF and HCC were decellularized, and evaluation of decellularization was done using morphological, histological and DNA analysis examination. Also, immunohistochemical staining using collagen, laminin, fibronectin and alphafetoprotein was done. Deposition area and intensity of the used immunohistochemical staining in liver capsules and the staining deposition thickness in the blood vessels and hepatic capsule walls were measured for comparison between the three models. RESULTS: Normal, HF and HCC livers were decellularized efficiently as confirmed by histological and DNA estimation. HCC decellularized samples showed significantly higher collagen, fibronectin and laminin deposition in both capsule and blood vessels, followed by HF decellularized samples, which also showed the highest thickness of laminin deposition in both capsule and blood vessels, then the normal model, which recorded the lowest value. Alphafetoprotein positive cells were absent in normal and HF, with rare cells in HCC. CONCLUSIONS: Even pathologic livers, HF and HCC, can be efficiently decellularized, showing normal morphology and architecture. However, HCC and HF showed significantly higher deposition of extracellular matrix proteins: collagen, fibronectin and laminin. The impact of these differences on physiological and immunological functions of the bioscaffold requires recellularization experiments.