Annals of clinical and laboratory science
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Ann. Clin. Lab. Sci. · Jan 2015
Cyclophosphamide Combined with Bone Marrow Mesenchymal Stromal Cells Protects against Bleomycin-induced Lung Fibrosis in Mice.
To examine the effects and possible mechanism of the immunosuppressant agent cyclophosphamide (CP) combined with bone marrow mesenchymal stromal cells (BM-MSCs) on bleomycin induced lung fibrosis in mice. ⋯ It was concluded that CP alone does not improve PF and may be harmful. In contrast, combined application of BM-MSCs with CP provided better protection against PF and may serve as an effective therapy.
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Ann. Clin. Lab. Sci. · Jan 2007
Effects of intrathecal injection of prednisolone acetate on expression of NR2B subunit and nNOS in spinal cord of rats after chronic compression of dorsal root ganglia.
N-methyl-D-aspartate receptor subunit 2B (NR2B) and neuronal nitric oxide synthase (nNOS) play important roles in the mechanism of neuropathic pain. To elucidate how glucocorticoids affect this mechanism, we studied the effects of intrathecal (it) injection of prednisolone acetate (PA) on a nociceptive stimulus and the changes of nNOS and NR2B subunit expression in the spinal dorsal horn of Sprague Dawley rats following chronic compression of the dorsal root ganglia (CCD). Paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured for 15 days postoperatively. ⋯ Chronic compression of the dorsal root ganglia induced time-dependent upregulation of nNOS and NR2B subunits of N-methyl-D-aspartate receptor within the spinal cord dorsal horn ipsilateral to CCD. Both upregulations were significantly diminished by it administration of PA (2.0 mg/kg), but not by lower doses of PA (0.5 or 1.0 mg/kg). The results suggest that PA upregulation of neuronal nitric oxide synthase and NR2B subunit expression in the spinal dorsal horn contributes to PA inhibition of hyperalgesia induced by chronic compression of dorsal root ganglia.
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Positive pressure ventilation with hyperdistention of the lungs (PPVHDL) causes microscopic lung injury in rats and in mice. This study compared lung lavage and serum levels of lactate dehydrogenase (LDH), aspartate aminotransferase (AST), creatinine phosphokinase (CPK), lung lavage and plasma endothelin-1 (ET-1) concentration, lung tissue ET-1 mRNA expression, angiotensin converting enzyme (ACE) activity of lung homogenates, and histology of the lung structure in control and PPVHDL rats. Rats were anesthetized with pentobarbital. ⋯ No significant difference was found in lung tissue ET-1 mRNA expression and lung protein concentration between the two groups. Lung ACE activity, in contrast, was significantly lower in PPVHDL rats. This study demonstrated that moderate alveolar hyperdistention caused significant structural lung damage accompanied by decreased ACE activity after seven hours of mechanical ventilation and that elevated lung lavage and serum LDH and AST levels in lung lavage and in serum might be early markers of ventilator-induced lung injury in this rat model.
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Ann. Clin. Lab. Sci. · Jan 2005
Swimming exercise training prior to acute myocardial infarction attenuates left ventricular remodeling and improves left ventricular function in rats.
The effect of exercise training prior to acute myocardial infarction (AMI) on left ventricular (LV) remodeling is poorly understood. This study investigated the protective effect of 3 weeks of swimming exercise training prior to AMI on cardiac morphology and function. Male Sprague-Dawley rats (n = 35) were randomly assigned to 3 groups: swimming training (n = 14, 90 min, 5 days/wk, 3 wk), sedentary (n =14), and controls (n = 7, no exercise, no MI). ⋯ Both LV-shortening fraction (SF%) and fractional area change (FAC%) were higher in the trained animals 4 wk post-AMI (39+/-12% vs 23+/-8%; p 0.002, and 48+/-14% vs. 38+/-9%; p 0.07, respectively). In conclusion, 3 wk of swimming exercise training prior to AMI significantly attenuated LV remodeling and improved LV function, despite no changes in LV dimensions or systolic function at the end of the exercise session. The data suggest that even a short-term training period is sufficient to induce cardiac protection.