RESUMEN
Aim To investigate the effect of Medi- coscab Tincture could increase the healing rate of burn coscab Tincture on the wound repair of deep partial thickness burn in rats and its possible mechanism. Methods SD100 rats were used to make a rat model of deep partial thickness burn. The rats were randomly divided into five groups; normal, model control, positive control, Medicoscab Tincture high-dose, and Medicoscab Tincture low-dose. The dosing group was changed daily for 14 consecutive days. The healing rate and water content of wound were measured at 3 d, 7 d and 14 d after burn. The activities of superoxide dismutase (SOD) and catalase (CAT) and the content of malondialdehyde ( MDA) were determined by bio-chemical analysis. Serum levels of tumor necrosis fac- tor-a (TNF-a), interleukin-1 (3 (IL-1(3) and interleu- kin-6 (IL-6) in rats were determined. Results Medi- wound and decrease the water content of burn wound tissue in rats ( P < 0. 05 ). The activity of SOD significantly increased, the content of MDA decreased (P < 0. 05), and the contents of TNF-a, IL-1 (3 and IL-6 in serum of burned rats decreased ( P < 0. 05, P < 0.01). Conclusions Medicoscab Tincture can improve the wound healing rate, reduce the wound water content, increase SOD activity, reduce the content of MDA in the wound, and reduce the serum levels of inflammatory factors TNF-a, IL-1 (3 and IL-6. Therefore, Medicoscab Tincture has a protective effect on deep partial thickness burn in rats.
RESUMEN
The present study was aimed at determining the effects of Tongqiao Huoxue Decoction (TQHXD) on the Ca(2+)-CaMKII-CREB pathway and the memory and learning capacities of rats with vascular dementia (VD). The rat VD model was established by using an improved bilateral carotid artery ligation method. The Morris water maze experiment was used to evaluate the ethology of the VD rats following treatments with TQHXD at 3.01, 6.02, and 12.04 g·kg(-1) per day for 31 days. At the end of experiment, the hippocampus were harvested and analyzed. Western blotting and RT-PCR were used to measure the expression levels of calmodulin-binding protein kinase II(CaMKII), protein kinase A(PKA), cAMP-response element binding protein(CREB), and three N-methyl-D-aspartic acid receptor subunits (NR1, NR2A, and NR2B). Our results revealed that TQHXD could alleviate the loss of learning abilities and increase the memory capacity (P < 0.05 and P < 0.01 vs the model group, respectively). The treatment with 6.02 and 12.04 g·kg(-1) of TQHXD significantly up-regulated the Ca(2+)-CaMKII-CREB pathway in the hippocampus. In conclusion, TQHXD showed therapeutic effects on a bilateral carotid artery ligation-induced vascular dementia model, through the up-regulation of calcium signalling pathways.