Int J Clin Exp Patho
-
Int J Clin Exp Patho · Jan 2015
Bone marrow mesenchymal stem cells ameliorate neurological deficits and blood-brain barrier dysfunction after intracerebral hemorrhage in spontaneously hypertensive rats.
Spontaneous intracerebral hemorrhage (ICH) is a common and fatal subtype of stroke, with hypertension the most common cause of this disorder. Bone marrow derived mesenchymal stem cells (BM-MSCs) have been shown to elicit protective properties in stroke models. In the present study, male spontaneously hypertensive rats (SHR) were subjected to ICH by intracerebral injection with autologous blood, Wistar-Kyoto (WKY) rats were employed as control. ⋯ Taken together, our results suggest that intravenously transplanted BM-MSCs exert therapeutic effects on ICH in spontaneously hypertensive rats. The underlying mechanisms are associated with the enhanced neurological function recovery and increased integrity of BBB. Our results provide the increased understanding of the underlying mechanisms and perspective of BMSCs in treatment for stroke.
-
Int J Clin Exp Patho · Jan 2015
Ruscogenin exerts beneficial effects on monocrotaline-induced pulmonary hypertension by inhibiting NF-κB expression.
This study aims to examine the effect of ruscogenin on pulmonary arterial hypertension (PAH) and to determine the mechanism underlying this effect. We isolated pulmonary vascular smooth muscle cells (PVSMCs) from the pulmonary artery of the rats; the PVSMCs were cultured in vitro and then were treated with platelet-derived growth factor (PDGF), PDGF + ruscogenin, or PDGF + ruscogenin + parthenolide. We randomized Sprague-Dawley rats into five groups as follows: control group, PAH group, low-dose group, medium-dose group, and high-dose group; the rats in the low-, medium-, and high-dose groups received the vehicle and ruscogenin 0.1, 0.4, and 0.7 mg/kg, respectively, from day 1 to day 21 after injection of monocrotaline (MCT). ⋯ We examined the levels of the nuclear factor kappa B (NF-κB) protein by using immunohistochemistry and western blot analysis, and the mRNA levels of NF-κB in PVSMCs were evaluated using real-time polymerase chain reaction (PCR). The mPAP, RVSP, and PAWT and the protein and mRNA levels of NF-κB were significantly higher in the PAH model group than in the control group (P < 0.05). Ruscogenin induced a significant dose-dependent decrease in the mPAP, RVSP, and PAWT and in the NF-κB expression in the PAH group (P < 0.05), which suggests that ruscogenin will also exert dose-dependent effects on MCT-induced PAH through the inhibition of NF-κB.
-
Int J Clin Exp Patho · Jan 2015
Resveratrol attenuates spinal cord injury-induced inflammatory damage in rat lungs.
Spinal cord injury (SCI)-induced systemic inflammatory response affects multiple organs outside the spinal cord. Treatment options for such complications are lacking. We studied the potential protective effects of resveratrol on SCI-induced inflammatory damage in rat lungs. ⋯ Resveratrol significantly reduced neutrophil infiltration and production of inflammatory mediators. Resveratrol treatment was accompanied by up-regulation of expression of SIRT1 and suppression of NF-κB activity in pulmonary tissues. These data suggest that resveratrol may protect the lungs from SCI-induced inflammatory damage, and could be used as a therapeutic option against pulmonary problems after SCI.
-
Int J Clin Exp Patho · Jan 2015
Ulinastatin mediates protection against vascular hyperpermeability following hemorrhagic shock.
Recent studies have suggested that intrinsic apoptotic signaling cascade is involved in endothelial barrier dysfunction following hemorrhagic shock (HS), which results in vascular hyperpermeability. Our previous study demonstrated that ulinastatin (UTI) inhibits oxidant-induced endothelial hyperpermeability and apoptotic signaling. In present study, we hypothesized that UTI would improve HS-induced vascular hyperpermeability by regulating the intrinsic apoptotic signaling cascade. ⋯ UTI inhibits vascular hyperpermeability following HS. UTI regulates oxidative stress and intrinsic apoptotic signaling following HS.
-
Int J Clin Exp Patho · Jan 2014
ReviewClarifying the nomenclature of intervertebral disc degeneration and displacement: from bench to bedside.
As a significant determinant of low back pain, intervertebral disc degeneration (IDD) has attracted more and more attention of both investigators and physicians. Disc herniation, termed as intervertebral disc displacement, is amongst the most prevalent spinal diseases closely linked with IDD. Due to the same origins and similar pathophysiology, the ambiguity regarding the similarity and difference of IDD and intervertebral disc displacement thus remains. ⋯ Collectively, IDD is a type of multifaceted, progressive spinal disease with or without clinical symptoms as back pain, characterized by extracellular matrix and the integrity of NP and AF lost, fissures formation. Disc herniation (termed as intervertebral disc displacement) is a type of spinal disease based on IDD or not, with local pain and/or sciatica due to mechanical compression and autoimmune cascades upon the corresponding nerve roots. Clarifying the nomenclature of intervertebral disc degeneration and displacement has important implications both for investigators and for physicians.