RESUMEN
Xuebijing (XBJ) injection is a herbal medicine that has been widely used in the treatment of sepsis in China; however, its role in the development and progression of Acinetobacter baumannii sepsis and the underlying mechanisms remain uninvestigated. In the present study, fifty-four male Wistar rats were randomly assigned to normal-control group, sepsis-control group, and sepsis + XBJ group, each containing three subgroups of different treatment time periods (6, 12, and 24 hrs following injection, resp.). The sepsis model was established by intraperitoneal injection of A. baumannii ATCC 19606. For XBJ treatment, 4 mL/kg XBJ was administrated simultaneously by intravenous injection through caudal vein every 12 hrs. All animals demonstrated ill state, obvious intestinal dysfunction, histopathological lung damages, and overactive inflammatory responses after A. baumannii infection, and these events could be partially reversed by XBJ treatment from the beginning of infection. XBJ induced an increase in the expression of anti-inflammatory mediator annexin A1; however, two proinflammatory cytokines, interleukin-8 (IL-8) and tumor necrosis factor- α (TNF- α ), were decreased at the each monitored time point. These findings suggested that XBJ via its cytokine-mediated anti-inflammatory effects might have a potential role in preventing the progression of A. baumannii infection to sepsis by early administration.
RESUMEN
The relationship between activities of chitinase and beta-1,3-glucanase and resistance to rhizomania of sugar beet were studied in diseased soil and disease-free soil by using a method of comparative physiology. Two resistant varieties and two susceptible ones of sugar beet were used in this experiment. Chitinase and beta-1,3-glucanase activities of the resistant varieties were higher than the susceptible ones in either diseased soil or disease-free soil. There is a positive correlation between chitinase, beta-1,3-glucanase activity and yield of beet in diseased soil, suggesting that pathogen infection can induce resistance to rhizomania through activating chitinase and beta-1,3-glucanase.