Current Issue : October - December Volume : 2014 Issue Number : 4 Articles : 5 Articles
Paraquat, a widely used herbicide, is well known to exhibit oxidative stress and lung injury. In the present study, we investigated the\npossible underlying mechanisms of cannabinoid receptor-2 (CB2) activation to ameliorate the proinflammatory activity induced by\nPQ in rats. JWH133, a CB2 agonist, was administered by intraperitoneal injection 1 h prior to PQ exposure. After PQ exposure for 4,\n8, 24, and 72 h, the bronchoalveolar lavage fluid was collected to determine levels of TNF-???? and IL-1????, and the arterial blood samples\nwere collected for detection of PaO2 level. At 72 h after PQ exposure, lung tissues were collected to determine the lung wet-to-dry\nweight ratios,myeloperoxidase activity, lung histopathology, the protein expression level of CB2, MAPKs (ERK1/2, p38MAPK, and\nJNK1/2), andNF-????Bp65. After rats were pretreated with JWH133, PQ-induced lung edema and lung histopathological changes were\nsignificantly attenuated. PQ-induced TNF-???? and IL-1???? secretion in BALF, increases of PaO2 in arterial blood, andMPOlevels in the\nlung tissue were significantly reduced. JWH133 could efficiently activate CB2, while inhibiting MAPKs and NF-????B activation. The\nresults suggested that activating CB2 receptor exerted protective activity against PQ-induced ALI, and it potentially contributed to\nthe suppression of the activation of MAPKs and NF-????B pathways....
Functionalized MWCNTs are used in many commercial and biomedical applications, but their potential health effects are not\nwell defined. We investigated and compared cytotoxic, genotoxic/oxidative, and inflammatory effects of pristine and carboxyl\nMWCNTs exposing human respiratory (A549 and BEAS-2B) cells to 1ââ?¬â??40 ?g/mL of CNTs for 24 h. Both MWCNTs induced low\nviability reduction (by WST1 assay) in A549 cells and only MWCNTs-COOH caused high viability reduction in BEAS-2B cells\nreaching 28.5% viability at 40 ?g/mL. Both CNTs induced membrane damage (by LDH assay) with higher effects in BEAS-2B\ncells at the highest concentrations reaching 20% cytotoxicity at 40 ?g/mL. DNA damage (by Fpg-comet assay) was induced by\npristine MWCNTs in A549 cells and by both MWCNTs in BEAS-2B cells reaching for MWCNTs-COOH a tail moment of 22.2\nat 40 ?g/mL versus 10.2 of unexposed cells. Increases of IL-6 and IL-8 release (by ELISA) were detected in A549 cells exposed\nto MWCNTs-COOH from 10 ?g/mL while IL-8 increased in BEAS-2B cells exposed to pristine MWCNTs at 20 and 40 ?g/mL.\nThe results show higher cytogenotoxicity of MWCNTs-COOH in bronchial and of pristine MWCNTs in alveolar cells. Different\ninflammatory response was also found. The findings suggest the use of in vitro models with different end points and cells to study\nCNT toxicity....
Background. Respiratory symptoms are usually underestimated in patients with chronic kidney disease undergoing maintenance\nhemodialysis. Therefore, we set out to investigate the prevalence of patients chronic dyspnea and the relationship of the symptom\nto lung function indices. Methods. Twenty-five clinically stable hemodialysis patients were included.The mMRC dyspnea scale was\napplied before and after hemodialysis. Spirometry, single breath nitrogen test, arterial blood gases, static maximum inspiratory\n(P1 max) and expiratory (Pe max) muscle pressures, and mouth occlusion pressure (P0.1) were also measured. Results. Despite normal\nspirometry, all patients (100%) reported mild to moderate degree of chronic dyspnea pre which was reduced after hemodialysis.The\nsole predictor of (?) mMRCwas the (?) P0.1 (r = 0.71, P< 0.001). The Pi max was reduced before and correlated with the duration\nof hemodialysis (r = 0.614, P < 0.001), whilst after the session it was significantly increased (P < 0.001). Finally (?) weight was\ncorrelated with the (?) Pi max %pred (P = 0.533, P = 0, 006) and with the (?) CV (%pred) (r = 0.65, P < 0.001). Conclusion.\nWe conclude that dyspnea is the major symptom among the CKD patients that improves after hemodialysis. The neuromechanical\ndissociation observed probably is one of the major pathophysiologic mechanisms of dyspnea....
Group 3 pulmonary hypertension (PH) is a common complication of chronic lung disease (CLD), including chronic obstructive\npulmonary disease (COPD), interstitial lung disease, and sleep-disordered breathing. Development of PH is associated with poor\nprognosis and may progress to right heart failure, however, in the majority of the patients with CLD, PH is mild to moderate and\nonly a small number of patients develop severe PH. The pathophysiology of PH in CLD is multifactorial and includes hypoxic\npulmonary vasoconstriction, pulmonary vascular remodeling, small vessel destruction, and fibrosis. The effects of PH on the right\nventricle (RV) range between early RVremodeling, hypertrophy, dilatation, and eventual failurewith associated increasedmortality.\nThe golden standard for diagnosis of PH is right heart catheterization, however, evidence of PH can be appreciated on clinical\nexamination, serology, radiological imaging, and Doppler echocardiography. Treatment of PH in CLD focuses on management\nof the underlying lung disorder and hypoxia. There is, however, limited evidence to suggest that PH-specific vasodilators such as\nphosphodiesterase-type 5 inhibitors, endothelin receptor antagonists, and prostanoids may have a role in the treatment of patients\nwith CLD and moderate-to-severe PH....
Cholinergic anti-inflammatory pathway (CAP) bridges immune and nervous systems and plays pleiotropic roles in modulating\ninflammation in animal models by targeting different immune, proinflammatory, epithelial, endothelial, stem, and progenitor\ncells and signaling pathways. Acute lung injury (ALI) is a devastating inflammatory disease. It is pathogenically heterogeneous\nand involves many cells and signaling pathways. Here, we emphasized the research regarding the modulatory effects of CAP on\nanimal models, cell population, and signaling pathways that involved in the pathogenesis of ALI. By comparing the differential\neffects of CAP on systemic and pulmonary inflammation, we postulated that a pulmonary parasympathetic inflammatory reflex is\nformed to sense and respond to pathogens in the lung.Work targeting the formation and function of pulmonary parasympathetic\ninflammatory reflex would extend our understanding of how vagus nerve senses, recognizes, and fights with pathogens and\ninflammatory responses....
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