ABSTRACT
Objective To study the effect of Interleukin-22 (IL-22) on murine asthmatic airway inflammation and airway remodeling, observe the effect of budesonide on IL-22 of asthmatic mouse model, explore the mechanism of budesonide in the treatment of asthma.Methods Ovalbumin(OVA) was used as an allergen to sensitize and challenge the mice.24 female specific-free (SPF) BALB/c mice aged four weeks were randomly divided into 3 groups:control group, asthma group and budesonide treatment group (BUD group).For Histopathological Examination, HE staining was used to measure the inflammation scores, AB-PAS staining was used to measure the hyperplasia of goblet cells and mucin.Enzyme-linked immunosorbent assay(ELISA) was used to analyze IL-22 levels in bronchoalveolar lavage fluid (BALF).Quantitative Real-time PCR was performed to analyze the effects of budesonide on IL-22 mRNA levels in lung tissue.Results The inflammation scores of asthma group were elevated compared with the control group.An overall change towards less severe asthmatic airway inflammation by the end of the trial was observed in the BUD group.IL-22 levels in BALF were significant decreased after the treatment of budesonide, the mRNA levels of IL-22 were obviously decreased in BUD group, too.A significant positive correlation was observed between the mRNA levels of IL-22 and airway inflammation.Conclusions The increasing IL-22 secretion can lead to the occurrence of airway inflammation of asthma.Budesonide can inhibit the expression of IL-22, thereby Budesonide could inhibit the development of airway inflammation of asthma.
ABSTRACT
Objective To establish and evaluate the CaV1?1?R528H gene knock?in mouse model of thyrotoxic hy?pokalemic periodic paralysis. Methods Thirty?six 8?week?old male CaV1?1?R528H gene knock?in mice and thirty?six 8?week?old wild?type male C57BL/6J mice were used in this study. Using three?factor two?level 2 × 2 × 2 factorial design ( the three factors including mutation, thyroxine and insulin, and two levels were with or without) , the mice were divided into 8 groups. The thyroxine groups were intraperitoneally injected with levothyroxine in a dose of 350 μg/kg once per day for 12 consecutive days to produce thyrotoxicosis. The insulin groups were intraperitoneally injected with short?acting insulin in a dose of 0?8 U/kg after the last administration of levothyroxine, and the potassium levels of different groups were meas?ured and recorded before (0 min) and after insulin injection (30 min, 60 min). Results (1) Compared with the control group, the following phenomena including irritability, dull coat, increased diet and water intake, and slow body weight gain, were observed in the thyrotoxic mice. Thyroid function tests showed that the levels of T3 and T4 in the thyrotoxic mice were significantly higher than those in the corresponding control mice (P<0?05), and the TSH level was significantly low?er than that of the corresponding control mice (P<0?05 ). (2) After administration of insulin or thyroxine alone, the po?tassium levels in the mutant and wild?type mice were not significantly different. However, after combined administration of thyroxine and insulin, the potassium levels in the mutant group were significantly lower than those in the wild?type mice at 30 min and 60 min ( P<0?05 for both). (3) The main effects and interactions:Mutation factor or thyroxine factor alone did not influence on the potassium level, only insulin showed hypokalemic effect (P<0?05). There were interactions be?tween thyroxine and mutation, and between insulin and mutation (P<0?05), but no interaction between thyroxine and in?sulin. Conclusions (1) A thyrotoxicosis state in mice is successfully developed in this study. (2) An CaV1?1?R528H gene knock?in mouse model of thyrotoxic hypokalemic periodic paralysis is successfully established.