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Issue 01
Ling Jiang1, Yan Tan2, JieTian1, Hong-Yu Ma2, Jin-Tao Li3*, Chao-Zhi Luo1*
Ibrain 2015;1(1):1-8 Download
Abstract
Backround: Stroke-associated pneumonia (SAP) is the most common complication after stroke, which increases the long-term mortality. In the acute phase of brain ischemia, obvious pathological injury is observed, which act as a main inducer for SAP. In this study, we sought to investigate the pathological changes following brain ischemia at each pulmonary lobe. Methods: Transient middle cerebral artery occlusion (tMCAO) was applied as a model of cerebral ischemia/reperfusion (I/R) injury (CIRI). Zea-Longa neurological deficit score was assessed at 24h post-injury and TTC staining was used to confirm the successful establishment of model. Histology and lung water content of each pulmonary lobe were conducted to evaluated the degree of lung injury. Results: Anatomy revealed that pulmonary lobes were divided into five single lobes. The posterior lobe of right lung gained the lowest histopathologic score while the highest water content was observed in left single lobe. Conclusions: Therefore, different pulmonary lobes may differ in the degree of lung injury induced by brain ischemia. This provide a novel and rigorous method for the study of lung injury.
Liuling Xiong
Biomed Res Int. 2015;2015:189292. Epub 2015 Nov 19. Download
Abstract
For cardiomyocytes, stretch is most important, activating oncogenes, protein kinases and possibly the inositol phosphate pathway, with regulation by the balance of angiotensin II, TGF-beta 1 and IGF-1, but not FGFs.Transforming growth factor-beta/bone morphogenetic protein (TGF-beta/BMP) signaling pathway is essential for embryonic and postnatal heart development and remodeling.Transforming Growth Factor (TGF)-β is markedly induced and rapidly activated in the infracted myocardium. Experimental studies suggest that TGF- beta 1 plays a pivotal role in the development of cardiac hypertrophy and heart failure,it can act with angiotensin II (Ang II), via activation of the angiotensin type 1 (AT1) receptor in cardiac myocytes and fibroblasts,then through Smad-dependent and Smad-independent pathways,as part of a signaling network in order to promote cardiac remodeling, which is a key determinant of clinical outcome in heart disease. TGF- beta 1 induces the proliferation of cardiac fibroblasts and their phenotypic conversion to myofibroblasts, the deposition of extracellular matrix (ECM) proteins such as collagen, fibronectin, and proteoglycans, and hypertrophic growth of cardiomyocytes.Moreover,recent studies have begun to reveal critical roles of TGF- beta –regulated-microRNAs (miRNAs) in the pathogenesis of cardiac hypertrophy and dysfunction. In this review we summarize the current knowledge,how TGF- beta 1 affected the pathogenesis of cardiac hypertrophy and dysfunction,as well as other relative studies on the TGF- beta 1.
De-Yi Zheng1, Jiao Jin2, Ting-hua Wang*3
Evid Based Complement Alternat Med. 2015;2015:626028. Epub 2015 Nov 17. Download
Abstract
Acute lung injury (ALI), induced by intestinal ischemia/reperfusion (II/R), has high incidence and mortality. It has been reported that iterleukin-1β (IL-1β) was essential for the full development of ALI induced by II/R, whereas the detailed regulating mechanism remains to be unclear. In this study, we found that the level of pulmonary edema at 16 hours post operation (hpo) was obviously enhanced than 8hpo and sham groups indicated by the dry/ wet from lung. Whereas, rats with II/R have the highest translation level for IL-1β and P38 MAPK in lung tissues at 16hpo, compare with 8hpo rats and sham groups, indicating by western blotting. Moreover, SB239063 administration, an inhibitor of P38 MAPK, protects effectively lung tissues from injury in intestinal ischemia reperfusion rats, and the molecular mechanism is associated with downregulation of mRNA expression of IL-1β, when compared with only II/R groups. Our findings indicated that P38 MAPK may regulate IL-1β to influence the consequence of ALI in rats subjected to II/R.
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