Objective To observe the fibroblast growth factor 21 ( FGF21 ) mRNA expression level in rat liver with non-alcoholic fatty liver disease ( NAFLD ) and to investigate its relationship with fat deposition and insulin resistance . Methods Forty SD male rats were randomly divided into the control group (n=10, NC group) fed with basic food and high-fat group (n=30, HF group) fed with high-fat diet.After 8-week feeding, 10 rats were selected to observe whether the NAFLD models were built successfully in the HF group .After that the rest of rats in the HF group were fed with high-fat diet, and at week 12, 10 rats were selected and at week 24, the other 10 were selected.The fasting blood-glucose (FPG), fasting insulin (FINS), alanine transamianse (ALT), aspartate transamianse (AST), total cholesterol (TC), triglyceride ( TG) , serum FGF21, serum FFA, and homeostasis model assessment of insulin resistance ( HOMA-IR) were calculated.The pathological change of liver was observed by HE staining;liver triglyceride ( TG) content was tested and the expression of FGF21 mRNA in liver was detected by RT-PCR.Results At the 8 th week, the body mass, liver-wet weight, serum TG and TC of the HF group were higher than those of the NC group (all P<0.05), liver tissues of the HF group changed to bullous steatosis and had inflammatory cell infiltration and spotty necrosis , so that NAFLD model was built successfully.In the end of 12 and 24th weeks, the serum FFA, TG content and HOMA-IR were significantly higher than those of the 8th week, and the 24th week was also higher than the 12th week (all P<0.05).During the week 8-12, the serum FGF21 and expression of FGF21 mRNA in liver of the HF group increased first and then decreased (all P<0.05). Conclusion The expression of FGF21 mRNA in liver and serum FGF21 of NAFLD rats were related with the liver TG con-tent.Besides, both of them have the same change in the early stage of NAFLD , and insulin resistance may inhibit the ex-pression of FGF21mRNA indirectly.

* Equal contribu- tors. Received November 6, 2014; Accepted January 21, 2015; Epub February 15, 2015; Published February 28, 2015 Abstract: Objective: We investigated the effect of xuesaitong on intestinal barrier dysfunction and related mecha- nisms in a rat model for intestinal ischemia-reperfusion. Methods: Rats were divided into sham-operated, disease- model and Xuesaitong-treated groups. In the disease-model and Xuesaitong-treated rats an intestinal ischemia- reperfusion injury (IRI) model was introduced, which was created by a temporary obstruction of the superior mes- enteric artery (SMA). The xuesaitong group was pre-treated with injections into the abdominal cavity prior to the generation of the IRI model. Tissue changes were evaluated using H&E staining and electron microscopy. Samples were analyzed at 0, 3 and 24 h post IRI. Ascites volumes as well as small intestinal mucosa bleeding, injury scores, wet to dry weight ratios, and propulsions were evaluated. Apoptotic rates were determined with TUNNEL assays. Blood serum tumor necrosis factor-α (TNF-α) levels were measured using ELISA, and Bcl-2 and caspase-3 expres- sion in small intestinal mucosa measured using immunohistochemistry. Results: We determined a significant in - crease of pathological damage to small intestinal tissues, intestinal wet to dry ratios, ascites volume, TNF-α levels, apoptosis rates of small intestinal mucosa, and expression of Bcl-2 and caspase-3 proteins in the disease-model group compared to the sham-operated group (P < 0.001), and intestinal motility was significantly decreased ( P < 0.001). However, comparisons between disease-model and xuesaitong pre-treated animals revealed, that in the treatment group these changes occurred in significant less severities. Conclusions: Xuesaitong can effectively allevi - ate intestinal barrier dysfunction caused by ischemia-reperfusion injury by reducing TNF-α, up-regulating Bcl-2 and down-regulating caspase-3 expression, in addition to increasing peristalsis.

OBJECTIVE:We investigated the effect of xuesaitong on intestinal barrier dysfunction and related mechanisms in a rat model for intestinal ischemia-reperfusion.METHODS:Rats were divided into sham-operated, disease-model and Xuesaitong-treated groups. In the disease-model and Xuesaitong-treated rats an intestinal ischemia-reperfusion injury (IRI) model was introduced, which was created by a temporary obstruction of the superior mesenteric artery (SMA). The xuesaitong group was pre-treated with injections into the abdominal cavity prior to the generation of the IRI model. Tissue changes were evaluated using H&E staining and electron microscopy. Samples were analyzed at 0, 3 and 24 h post IRI. Ascites volumes as well as small intestinal mucosa bleeding, injury scores, wet to dry weight ratios, and propulsions were evaluated. Apoptotic rates were determined with TUNNEL assays. Blood serum tumor necrosis factor-α (TNF-α) levels were measured using ELISA, and Bcl-2 and caspase-3 expression in small intestinal mucosa measured using immunohistochemistry.RESULTS:We determined a significant increase of pathological damage to small intestinal tissues, intestinal wet to dry ratios, ascites volume, TNF-α levels, apoptosis rates of small intestinal mucosa, and expression of Bcl-2 and caspase-3 proteins in the disease-model group compared to the sham-operated group (P < 0.001), and intestinal motility was significantly decreased (P < 0.001). However, comparisons between disease-model and xuesaitong pre-treated animals revealed, that in the treatment group these changes occurred in significant less severities.CONCLUSIONS:Xuesaitong can effectively alleviate intestinal barrier dysfunction caused by ischemia-reperfusion injury by reducing TNF-α, up-regulating Bcl-2 and down-regulating caspase-3 expression, in addition to increasing peristalsis.

Objective To observe the effect of coffee on the expression of insulin receptor substance ( IRS)-1 and IRS-2 and their tyrosine/serine phosphorylation in rats with insulin resistance ( IR) and to evaluate its effect on the post-re-ceptor signal transduction in adipose tissues .Methods Totally 40 Wistar rats were randomly divided into the normal con-trol ( NC) group, caffeinated coffee lavage ( CC) group, decaffeinated coffee lavage ( DC) group, and IR ( IR) group, with 10 rats in each group .Except for NC group , the other three groups were given high fat diet .Meanwhile , CC and DC groups, respectively, were treated with caffeinated coffee and decaffeinated coffee daily lavage for 12 weeks.Then the oral glucose tolerance test (OGTT) was given and homeostasis model assessment of insulin resistance (HOMA-IR) was em-ployed to assess the degree of insulin resistance .The levels of IRS-1 and IRS-2 and their mRNA in adipose tissues were de-tected by RT-PCR.And the tyrosine/serine phosphorylation was measured by Western blotting .Results IR group had higher blood glucose levels at the time of 60 and 120 min as compared with NC group (P<0.05, P<0.01, respectively). CC, DC, and IR groups displayed higher fasting insulin levels than NC group (all P<0.05).However, HOMA-IRs of CC, DC, and NC groups were all significantly lower than that of IR group (all P<0.05).Although no significant differ-ences were found in the levels of IRS-1 and IRS-2 as well as IRS-2 mRNA among the four groups (P>0.05), IRS-1 mR-NA of the NC and CC groups was higher than that of the IR group (all P<0.01).Higher tyrosine phosphorylation and low-er serine phosphorylation were exhibited in NC , CC, and DC groups as compared with the IR group (all P<0.05).Con-clusions Insulin resistance induced by high fat diet could be alleviated by coffee , whose mechanism may be explained by its effect on post-receptor signal transduction in adipose tissues by the alteration of IRS-1 mRNA as well as its tyrosine/ser-ine phosphorylation .

本文就禽类感染禽流感的预防措施的关键点,从病原特征、防控技术等方面进行了分析和阐述,为能有效的控制和预防禽流感及其流行提供了参考。

Objective To establish a subcutaneous xenograft model of human prostate carcinoma in nude mice.Methods PC-3 cells of the human prostate carcinoma were inoculated subcutaneously into the neck back of BAlB/c nude mice.The tumor incubation period,forming tumor percentage was calculated and pathological identification of tumors were carried out Results The mean incubation period of xenograft by inoculating subcutaneously with human prostate PC-3 cells was 24 days with 100% tumor forming.The time of tumor volume doubled was 10 days.Morphological and functional features of xenograft were basically same as original tumor.Conclusion The xenograft model of human prostate carcinoma established in this study could provide valuable experiment platform for radioimmunoimaging and radioimmunotherapy of the prostate carcinoma.

Objectives To investigate the effect of cellulose on the formation of aberrant crypt foci (ACF) in rats colon. Methods Forty-eight Wister male rats were randomized into 4 groups after one week acclimatization. The rats in group B and D were given 1, 2-climethylhydrazine (20 mg/kg) intra abdominally once a week until 10 weeks, whereas the rats in group A and C with the same volume of normal saline. The rats in group A and B were fed with standard forage whereas the rats in group C and D with forage containing 10% cellulose. At the 12th week, all the rats were sacrificed to examine the ACF in their colon. Results There were no significant differences in rat s weight gain and the length of colon among study groups. There were no abnormal lesions in viscera of all rats. The content of cecum in rats fed with cellulose was higher than that with standard forage, but there was no significant difference between the content of distal and proximal colon in all groups. The total number of ACF and the lesions that contained more than 4 crypts in colon of group D rats was significantly fewer than that of group B. Conclusions The cellulose could inhibit the formation of pre-cancerous lesion in colon of rats.

[Objective] To observe the effect of RDGLC on the ratio of small intestine propulsion,the secretion of gastric fluid acidity and pepsin of the healthy rat. [Methods] Healthy SD rats were divided randomly into saline.domperidone and different doses group of RDGLC. The effect of small intestine propulsion,the secretion of gastric fluid acidity,free acid,total acid and the pepsin were observed in all groups. [Results] The doses over 0. 5 mg/(kg ?time) of RDGLC could enhance small intestine propulsion; high dose of RDGLC could increase the secretion of gastric fluid acidity, free acid, total acid ;low, middle, high dose of ROGLC could promote the activity of pepsin. [Conclusion] ROGLC could promote the motion of small intestine, increase the secretion of gastric fluid acidity and pepsin, which might be one of the pharmacological basis for treating functional dyspepsia.

目的探讨低聚果糖对大鼠结肠癌前期病变—畸变隐窝病灶(ACF)形成的影响。方法 48只雄性Wister大鼠经适应性喂养1周后随机分为A、B、C和D组,每组12只,B、D组大鼠每周皮下注射1次二甲基肼(20 mg／kg),A、C组大鼠给予等量生理盐水,连续10周；同时A、B组大鼠给予标准鼠食,而C、D组大鼠给予含10％低聚果糖的鼠食,喂养至第12周处死,观察大鼠体重、结肠长度和ACF,以及结肠内容物重量及其丁酸含量的变化。结果各组大鼠体重增加及结肠长度差异无显著性,腹腔内脏器未见明显病灶。C、D组盲肠内容物重量显著高于A、B组,但各组近、远端结肠内容物重量差异无显著性。C、D组各肠段内容物丁酸浓度显著高于A、B组的相应肠段,D组≥4个隐窝的ACF数均显著低于B组,且丁酸浓度和ACF总数呈显著的负相关。结论低聚果糖能抑制大鼠结肠癌前期病变的形成。

目的观察獐乳对正常大鼠胃排空、小肠推进及对盐酸多巴胺致胃排空延迟模型大鼠胃排空的影响.方法采用 SD系大鼠,随机分为空白对照组、模型对照组、吗丁啉组和獐乳不同剂量组, 观察各组大鼠胃排空及小肠推进情况.结果獐乳低、中、高剂量组胃甲基橙残留率明显降低,能促进正常大鼠胃排空;獐乳中、高剂量组对正常大鼠小肠推进有促进作用;獐乳低、中、高剂量组均不能显著促进多巴胺所致大鼠胃排空延迟,胃内甲基橙残留率与模型对照组相比无显著降低.结论獐乳具有促胃肠动力作用,但其促进胃肠动力作用的机制可能不是通过阻断多巴胺受体途径.