Ulcerative colitis (UC) is considered a long-term inflammatory disorder worldwide. Its pathogenesis is associated with reduced antioxidant capacity. Lycopene (LYC) is a powerful antioxidant with strong free radical scavenging property. The present work has done to assess changes of colonic mucosa in induced UC and the possible ameliorative effects of LYC. Forty-five adult male albino rats were randomly divided into four groups: group I (control), group II was given 5 mg/kg/day (LYC) by oral gavage for 3 weeks. Group III (UC) was received single intra-rectal injection of acetic acid. Group IV (LYC+UC) received LYC in same dose and duration as before and acetic acid on 14th day of the experiment. UC group showed loss of surface epithelium with destructed crypts. Congested blood vessels with heavy cellular infiltration were observed. Significant decrease in goblet cell numbers and the mean area percentage of ZO-1 immunoexpression were noticed. Significant increase in the mean area percentage of collagen and the mean area percentage of COX-2 were also noticed. Ultrastructural changes were matched with light microscopic results that showed abnormal destructive columnar and goblet cells. Histological, immunohistochemical, and ultrastructural findings in group IV supported the ameliorative role of LYC against destructive changes induced by UC.

Nowadays, using electromagnetic devices (EMD) has been increased. However, the control of EMD hazards was poorly evaluated, especially those affected the hippocampus. Regular physical exercises are safe, easily, inexpensive, and acceptable for long-term use. It is reported that exercise protects against many health problems.
is to investigate the hypothesis of the possible prophylactic effect of exercise on the hippocampal damage induced by electromagnetic waves of Wi-Fi.
Adult male albino rats were divided into four groups: group I (control), group II (exercise), group III (Wi-Fi), and group IV (exercise -Wi-Fi). Hippocampi were subjected to biochemical, histological, and immunohistochemical techniques.
In group III, a significant increase in the oxidative enzymes as well as decrease in antioxidant enzymes were detected in rat hippocampus. Additionally, the hippocampus showed degenerated pyramidal and granular neurons. An evident decrease in both PCNA and ZO-1 immunoreactivity was also noticed. In group IV, physical exercise alleviates the effect of Wi-Fi on previously mentioned parameters.
Regular physical exercise performance significantly minimizes the hippocampal damage and protects against the hazarders of chronic Wi-Fi radiation exposure.

Leaky gut is a condition of increased paracellular permeability of the intestine due to compromised tight junction barriers. In recent years, this affliction has drawn the attention of scientists from different fields, as a myriad of studies prosecuted it to be the silent culprit of various immune diseases. Due to various controversies surrounding its culpability in the clinic, approaches to leaky gut are restricted in maintaining a healthy lifestyle, avoiding irritating factors, and practicing alternative medicine, including the consumption of supplements. In the current study, we investigate the tight junction-modulating effects of processed Aloe vera gel (PAG), comprising 5-400-kD polysaccharides as the main components. Our results show that oral treatment of 143 mg/kg PAG daily for 10 days improves the age-related leaky gut condition in old mice, by reducing their individual urinal lactulose/mannitol (L/M) ratio. In concordance with in vivo experiments, PAG treatment at dose 400 μg/mL accelerated the polarization process of Caco-2 monolayers. The underlying mechanism was attributed to enhancement in the expression of intestinal tight junction-associated scaffold protein zonula occludens (ZO)-1 at the translation level. This was induced by activation of the MAPK/ERK signaling pathway, which inhibits the translation repressor 4E-BP1. In conclusion, we propose that consuming PAG as a complementary food has the potential to benefit high-risk patients.

UNASSIGNED: Lung resection and one lung ventilation (OLV) during video-assisted thoracoscopic surgery (VATS) may lead to acute lung injury. Dexmedetomidine (DEX), a highly selective α2 adrenergic receptor agonist, improves arterial oxygenation in adult patients undergoing thoracic surgery. The aim of this pilot study was to explore possible mechanism related to lung protection of DEX in patients undergoing VATS.
UNASSIGNED: Seventy-four patients scheduled for VATS were enrolled in this study. Three timepoints (before anesthesia induction (T0), 40 min after OLV (T1), and 10 min after two-lung ventilation (T2)) of arterial blood gas were obtained. Meanwhile, lung histopathologic examination, immunohistochemistry analysis (occludin and ZO-1), levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in lung tissue and plasma, and activation of phosphoinositide-3-kinase (PI3K)/AKT/hypoxia-inducible factor (HIF)-1α signaling were detected. Postoperative outcomes including duration of withdrawing the pleural drainage tube, length of hospital stay, hospitalization expenses, and postoperative pulmonary complications (PPCs) were also recorded.
UNASSIGNED: Sixty-seven patients were randomly divided into DEX group (group D, n=33) and control group (group N, n=34). DEX improved oxygenation at T1 and T2 (group D vs group N; T1: 191.8 ± 49.8 mmHg vs 159.6 ± 48.1 mmHg, P = 0.009; T2: 406.0 mmHg [392.2-423.7] vs 374.5 mmHg [340.2-378.2], P = 0.001). DEX alleviated the alveolar capillary epithelial structure damage, increased protein expression of ZO-1 and occludin, inhibited elevation of the expression of TNF-α and IL-6 in lung tissue and plasma, and increased protein expression of p-PI3K, p-AKT and HIF-1α. Dex administered had better postoperative outcomes with less risk of PPCs and hospitalization expenses as well as shorter duration of withdrawing the pleural drainage tube and length of hospital stay.
UNASSIGNED: Activation of PI3K/Akt/HIF-1α signaling might be involved in lung protection of DEX in patients undergoing VATS.

BACKGROUND: We determined whether plasma concentrations of ZO-1 proteins may be used a predictor of sepsis severity and 30-day mortality.
METHODS: A total of 143 patients with sepsis and 30 healthy controls were enrolled. Plasma ZO-1 proteins concentrations were measured. Various methods, including area under the curves (AUCs), Kaplan-Meier curve, Cox regression, net reclassification improvement (NRI) and integrated discrimination improvement (IDI), were carried out to determine the value of ZO-1 in predicting 30-day mortality.
RESULTS: Plasma ZO-1 concentrations in patients with sepsis and septic shock were significantly higher than those in healthy controls and were associated with the number of organ failures. ZO-1 concentrations also correlated with APACHE II or SOFA score and predicted 30-day mortality in sepsis patients with an AUC of 0.754. Multivariable regression analyses showed that a ZO-1 concentration ≥2.60 ng/ml remained a significant predictor of 30-day mortality in sepsis patients. Kaplan-Meier survival plots showed that patients with ZO-1 concentrations <2.60 ng/ml had a clear survival benefit. Adding ZO-1 to the SOFA score significantly improved its prognostic accuracy.
CONCLUSIONS: Plasma ZO-1 proteins appear to be a valuable prognostic biomarker for the severity of sepsis and a predictor of 30-day mortality for patients with sepsis.

Fibrogenesis is a common feature for all types of chronic kidney disease (CKD). Epithelial-to-mesenchymal transition (EMT) of renal tubular epithelial cells is one of the main processes involving renal fibrosis and its inhibition is considered as a preventive/therapeutic strategy for CKD. Trigonelline (TRIG), a plant alkaloid commonly found in herbs, coffee bean, soy bean and other edible food plants, has several beneficial effects on human health and has been proposed to reduce renal fibrosis but with unclear mechanisms. This study thus addressed cellular mechanism underlying the anti-fibrogenic effects of TRIG in renal tubular epithelial cells grown in vitro. EMT was successfully induced by oxalate treatment as indicated by morphological changes into spindle-shape cells, increased expression of mesenchymal proteins (fibronectin, vimentin and α-smooth muscle actin (α-SMA)), decreased expression of epithelial proteins (E-cadherin and zonula occludens-1 (ZO-1)) and increased activity of a profibrotic factor (matrix metalloproteinase-9 (MMP-9)). Interestingly, these oxalate-induced EMT features could be attenuated by TRIG pretreatment. Moreover, TRIG also prevented oxalate-induced cell migration, reactive oxygen species (ROS) overproduction, and down-regulation of Nrf-2 signaling molecule. These data indicated that TRIG could attenuate the effects of oxalate-induced EMT and thus may serve as the anti-fibrotic compound for prevention and/or treatment of CKD.

The purpose of this study was to investigate the protective effects and mechanisms of the essential oil of Zanthoxylum bungeanum pericarp (ZBEO) on dextran sulfate sodium (DSS)-induced experimental colitis in mice. ZBEO decreased DSS-induced body weight loss, the disease activity index, colon length shortening, colonic pathological damage, and myeloperoxidase activities. The production of pro-inflammatory mediators was significantly alleviated by ZBEO. Further mechanistic analysis showed that ZBEO inhibited inflammation by regulating NF-κB and PPARγ pathways. ZBEO also inhibited NLRP3 activation in colitis in mice. Furthermore, ZBEO contributed to the maintenance of tight junction architecture by regulating the expression of zonula occludens-1 during colitis. Surprisingly, treatment with ZBEO increased levels of the commensal bacteria containing Lactobacillus and Bifidobacteria but reduced Escherichia coli levels in the feces of mice. These results suggested that supplementation with ZBEO might provide a new dietary strategy for the prevention of ulcerative colitis.

BACKGROUND: Increased intestinal permeability and altered expression of tight junction (TJ) proteins may be implicated in the pathogenesis of irritable bowel syndrome (IBS). This study aimed to investigate the expression of adherens junction (AJ) protein E-cadherin and TJ proteins zonula occludens (ZO)-1 and claudin (CLD)-1 and associations with IBS symptoms.
METHODS: Junctional proteins were immunostained in cecal biopsy tissue of Rome II IBS patients (n = 34) comprising both alternating (IBS-A) and diarrhea predominant (IBS-D) subtypes, and controls (n = 12). IBS symptom duration, abdominal pain severity and stool frequency were assessed for IBS patients. Protein expression was determined by immunofluorescence.
RESULTS: E-cadherin and ZO-1 protein expression was significantly lower (p = 0.03 and p = 0.016, respectively) in the cecal surface epithelium of the IBS group comprising both IBS-A and IBS-D subtypes. CLD-1 expression was not significantly altered compared with controls. On subtype analysis, ZO-1 expression was significantly reduced in both IBS-A and IBS-D compared with controls, whereas E-cadherin was reduced only in IBS-A. Lower E-cadherin expression was associated with longer symptoms duration specifically in IBS-A patients (rs = -0.76, p = 0.004). Reduced E-cadherin associated with abdominal pain severity in the overall IBS group (rs = -0.36, p = 0.041), but this association was unrelated to IBS subtype.
CONCLUSIONS: E-cadherin protein expression in the cecum was significantly lower in IBS-A compared with controls and associated with longstanding symptoms. E-cadherin was further associated with abdominal pain severity in the IBS group overall, but unrelated to IBS subtype. Altered E-cadherin expression may provide novel insights into mechanisms underlying intestinal barrier dysfunction in IBS.