Fenzan wu’s scientific contributions in er stress and endoplasmic reticulum anoxia tisular

[show abstract] [hide abstract] ABSTRACT: after spinal cord injury (SCI), the destruction of blood-spinal cord barrier (BSCB) is shown to accelerate gathering of noxious blood-derived components in the nervous system, leading to secondary neurodegenerative damages. SCI activates endoplasmic reticulum stress (ER stress), which is considered to evoke secondary damages of neurons and glia. Recent evidence indicates that dl-3-n-butylphthalide (NBP) has the neuroprotective effect in ischaemic brain injury, but whether it has protective effects on SCI or not is largely unclear. Here, we show that NBP prevented BSCB disruption after SCI via inhibition of ER stress.


Following a moderate contusion injury of the T9 level of spinal cord, NBP was administered by oral gavage and further treated once a day.Anoxia tisular NBP significantly attenuated BSCB permeability and breakdown of adherens junction (AJ) and tight junction (TJ) proteins, then improved locomotion recovery following SCI. The protective role of NBP on BSCB disruption is associated with the restrain of ER stress caused by SCI. Furthermore, NBP considerably constrained the expression of ER stress-associated proteins and degradation of TJ and AJ in human brain microvascular endothelial cells (hbmecs) treated with TG. In conclusion, our results indicate that ER stress is associated with the disruption of BSCB integrity after injury, NBP attenuates BSCB disruption via inhibiting ER stress and improve functional recovery following SCI.

[show abstract] [hide abstract] ABSTRACT: stem cell therapies are currently gaining momentum in the treatment of spinal cord injury (SCI).Anoxia tisular however, unsatisfied intrinsic neurite growth capacity constitutes significant obstacles for injured spinal cord repair and ultimately results in neurological dysfunction. The present study assessed the efficacy of thrombospondin-1 (TSP-1), a neurite outgrowth-promoting molecule, modified bone marrow mesenchymal stem cells (bmscs) on promoting neurite outgrowth in vitro and in vivo of oxygen–glucose deprivation (OGD) treated motor neurons and SCI rat models. The present results demonstrated that the treatment of bmscs+TSP-1 could promote the neurite length, neuronal survival, and functional recovery after SCI. Additionally, TSP-1 could activate transforming growth factor-β1 (TGF-β1) then induced the smad2 phosphorylation, and expedited the expression of GAP-43 to promote neurite outgrowth.Anoxia tisular the present study for the first time demonstrated that bmscs+TSP-1 could promote neurite outgrowth and functional recovery after SCI partly through the TGF-β1/p-samd2 pathway. The study provided a novel encouraging evidence for the potential treatment of bmscs modification with TSP-1 in patients with SCI.

[show abstract] [hide abstract] ABSTRACT: cerebrovascular disease such as stroke is one of the most common diseases in the aging population, and neural stem cells (nscs) transplantation may provide an alternative therapy for cerebral ischemia. However, a hostile microenvironment in the ischemic brain offers is challenging for the survival of the transplanted cells. Considering the neuroprotective role of basic fibroblast growth factor (bfgf), the present study investigated whether bfgf gene-modified nscs could improve the neurological function deficit after transient middle cerebral artery occlusion (MCAO) in adult male sprague–dawley rats.Anoxia tisular these rats were intravenously injected with modified nscs (5×10⁶/200 μl) or vehicle 24 h after MCAO. Histological analysis was performed on days 7 and 28 after tmcao. The survival, migration, proliferation, and differentiation of the transplanted modified C17.2 cells in the brain were improved. In addition, the intravenous infusion of nscs and bfgf gene-modified C17.2 cells improved the functional recovery as compared to the control. Furthermore, bfgf promoted the C17.2 cell growth, survival, and differentiation into mature neurons within the infarct region. These data suggested that bfgf gene-modified nscs have the potential to be a therapeutic agent in brain ischemia.

[show abstract] [hide abstract] ABSTRACT: spinal cord injury (SCI) possesses a significant health and economic burden worldwide.Anoxia tisular traumatic SCI is a devastating condition that evolves through two successive stages. Throughout each of these stages, disturbances in ionic homeostasis, local oedema, ischaemia, focal haemorrhage, free radicals stress and inflammatory response were observed. Although there are no fully restorative cures available for SCI patients, various molecular, cellular and rehabilitative therapies, such as limiting local inflammation, preventing secondary cell death and enhancing the plasticity of local circuits in the spinal cord, were described. Current preclinical studies have showed that fibroblast growth factors (fgfs) alone or combination therapies utilizing cell transplantation and biomaterial scaffolds are proven effective for treating SCI in animal models.Anoxia tisular more importantly, some studies further demonstrated a paucity of clinical transfer usage to promote functional recovery of numerous patients with SCI. In this review, we focus on the therapeutic capacity and pitfalls of the FGF family and its clinical application for treating SCI, including the signalling component of the FGF pathway and the role in the central nervous system, the pathophysiology of SCI and the targets for FGF treatment. We also discuss the challenges and potential for the clinical translation of FGF-based approaches into treatments for SCI.