The aim of this experimental study was to investigate the possible protective effects of dantrolene on traumatic spinal cord injury (SCI). Twenty-four New Zealand rabbits were divided into three groups: Sham (no drug or operation, n = 8), Control (SCI + 1 mL saline intraperitoneally (i.p.), n = 8), and DNT (SCI + 10 mg/kg dantrolene in 1 mL, i.p., n = 8). Laminectomy was performed at T10 and balloon catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated according to the Tarlov scoring system. Blood, cerebrospinal fluid and tissue sample from spinal cord were taken for measurements of antioxidant status or detection of apoptosis. After 4 h SCI, all animals in control or DNT-treated groups became paraparesic. Significant improvement was observed in DNT-treated group, 24 h after SCI, with respect to control. Traumatic SCI led to an increase in the lipid peroxidation and a decrease in enzymic or non-enzymic endogenous antioxidative defense systems, and increase in apoptotic cell numbers. DNT treatment prevented lipid peroxidation and augmented endogenous enzymic or non-enzymic antioxidative defense systems. Again, DNT treatment significantly decreased the apoptotic cell number induced by SCI. In conclusion, experimental results observed in this study suggest that treatment with dantrolene possess potential benefits for traumatic SCI.
In this study, the roles of IL-1beta, IL-6 and TNF-alpha in amyloid arthropathic chickens with variable amounts (severe, moderate and mild) of amyloid accumulation were investigated. The presence and the levels of cytokines were evaluated in serum and in joint tissues by using ELISA and immunohistochemistry, respectively. One hundred brown layer chicks were allocated into four groups and intra-articular injections of Freund's adjuvant were used to induce amyloid arthropathy in Groups II, III and IV. Vitamin A in group II, and methylprednisolone in Group IV were added to enhance and to reduce the severity of amyloidosis, respectively. At the end of the study, a positive correlation was observed among the incidence and severity of amyloidosis, the serum amyloid A levels and the IL-1beta values both in the serum and tissues. Elevation in the tissue TNF-alpha levels in parallel with the severity of amyloidosis has also been noted. As a conclusion, IL-1beta appears to play an important role in avian AA amyloidosis either alone or in combination with TNF-alpha. Further investigation is needed for understanding the role of the pro-inflammatory cytokines in avian AA amyloidosis.
The aim of this experimental study was to investigate the possible protective effect of dexmedetomidine (DEX) on traumatic spinal cord injury (SCI). Twentytwo New Zealand rabbits were divided into three groups: sham (no drug or operation, n = 6), Control [SCI ? single dose of 1 mL saline intraperitoneally (i.p), after trauma; n = 8] and DEX (SCI ? 1 lg/kg dexmedetomidine in 1 mL, i.p, after trauma, n = 8). Laminectomy was performed at T10 and balloon angioplasty catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated by an independent observer according to the Tarlov scoring system. Blood, cerebrospinal fluid (CSF), tissue samples from spinal cord were taken for biochemical and histopathological evaluations. After 4 h of SCI, all animals in control or DEX treated groups became paraparesic. On the other hand, 24 h after SCI, partial improvements were observed in both control and DEX treated groups. Traumatic SCI leads to increase in the lipid peroxidation and decreases enzymatic or nonenzymatic endogenous antioxidative defense systems. Again, SCI leads to apoptosis in spinal cord. DEX treatment slightly prevented lipid peroxidation and augmented endogenous antioxidative defense systems in CSF or spinal cord tissue, but failed to prevent apoptosis or neurodeficit after traumatic SCI. Therefore, it could be suggested that treatment with dexmedetomidine does not produce beneficial results in SCI.
Detrimental effects of aflatoxin B 1 (AFB 1 ) on the embryonic development of broiler tibia and its proximal growth plate were determined by means of histological, histometric and immunohistochemical methods. For this, 420 fertile eggs from parent stocks of Ross 308 broiler chickens were divided into five groups according to the proposed treatment: a control untreated group, a group injected with 30% ethanol and three further groups to be injected with 5 , 15 or 40 ng AFB 1 . The eggs were injected into the air space prior to incubation. Five eggs from each group were opened at 9, 11, 13, 17, 19 and 21 days of incubation and tibial tissue samples were removed, dissected of muscle and connective tissues, and processed by means of routine histological techniques. The cell proliferation rate of the epiphyseal growth plate cells was determined by immunohistochemical assay of proliferating cell nuclear antigen (PCNA) expression. The results showed that both proliferative and hypertrophic zones narrowed significantly (P B0.05), when compared with the controls, in all of the AFB 1 -treated groups whereas the transitional zone thickened, especially in the group given 40 ng AFB 1 group. The PCNA positivity indices of 15 and 40 ng AFB 1 -treated groups were significantly higher (P B0.05) on days 11, 13, 17, 19 and 21 of incubation. It was concluded that in ovoadministered AFB 1 adversely affected embryonic development of the tibial growth plate, and that affected hatched broilers might also be more susceptible to skeletal disorders during growth.
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