ABSTRACT
ObjectiveTo explore the effect of Jianpi Yichang power on the nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） inflammasome signaling pathway in a rat model of ulcerative colitis （UC）. MethodSixty Sprague-Dawley rats were randomly divided into a normal group （n=10） and an experimental group （n=50）. The experimental group received 5% dextran sulfate sodium （DSS） solution freely for 7 days to induce UC， and then they were further randomly divided into model group， sulfasalazine （0.3 g·kg-1） group， and high-， medium-， and low-dose Jianpi Yichang power groups （54.4， 27.2， 13.6 g·kg-1） for continuous treatment of 14 days. The general condition of the rats was observed and recorded daily， and the disease activity index （DAI） was scored before and after treatment. Enzyme-linked immunosorbent assay （ELISA） was used to detect the levels of interleukin-1β （IL-1β） and interleukin-18 （IL-18） in the serum of rats in each group. Hematoxylin-eosin （HE） staining was performed to observe the histopathological changes in the colon tissue. Immunohistochemistry， Western blot， and Real-time polymerase chain reaction （Real-time PCR） were used to detect the positive protein expression， protein expression， and mRNA expression of NLRP3， apoptosis-associated speck-like protein containing a CARD （ASC）， and cysteine aspartate-special proteases-1（Caspase-1） in the colon tissue. ResultCompared with the condition in the normal group， the general condition of rats in the model group was relatively poor， with increased DAI scores （P<0.01）， pathological changes in the colon， increased levels of IL-1β and IL-18 in the serum （P<0.01）， and enhanced positive protein expression， protein expression， and mRNA expression of NLRP3， ASC， and Caspase-1 in the colon tissue （P<0.01）. Compared with the condition in the model group， the general condition of rats in the Jianpi Yichang power groups at various doses improved significantly， with reduced DAI scores （P<0.05， P<0.01）， alleviated pathological changes in the colon as revealed by HE staining， and reduced protein expression levels of NLRP3 and Caspase-1 in the colon tissue （P<0.05， P<0.01）. The serum levels of IL-1β and IL-18， and ASC protein expression in the colon， as well as the mRNA expression levels of NLRP3， ASC， and Caspase-1， decreased in the high- and medium-dose Jianpi Yichang power groups （P<0.05， P<0.01）. The positive protein expression levels of NLRP3， ASC， and Caspase-1 were reduced in the high-dose Jianpi Yichang power group （P<0.01）. The positive protein expression levels of ASC and Caspase-1 were reduced in the medium-dose Jianpi Yichang power group （P<0.05）. The mRNA expression level of ASC was reduced in the low-dose Jianpi Yichang power group （P<0.05）. ConclusionJianpi Yichang power can reduce colon immune inflammatory damage by regulating the NLRP3 inflammasome signaling pathway， thereby exerting a role in treating UC.
ABSTRACT
Objective To observe the expressions of NeuN and pCaMKⅡα in brain and test the spacial learning and memory in neonatal hypoxic?ischemia encephalopathy ( HIE ) model mice. Methods 7d ICR mice were randomly divided into sham group( n=19) and model group( n=23). HIE model was induced by right common carotid artery ligation followed by 8% oxygen hypoxia for 100 min. DAPI staining was used to examine brain pathological change,immunofluorescent staining was used to examine the expression of NeuN and pCaMKⅡα in the ipsilateral brain,and Morris water maze was used to test the spa?cial learning and memory. Results Mice in sham group showed that brain cells were arranged in a dense and orderly manner,the number of NeuN?positive cells and pCaMKⅡα?positive cells were (106.50±20.07), (87.17±16.55) respectively in the brain,and the escape latency was short. Compared with mice in sham group,mice in model group showed more cells loss,less NeuN?positive cells(19.17±3.60) and less pCaMKⅡα?positive cells(13.33±3.62) in the ipsilateral hemisphere,and longer escape latency(P<0.01). Conclu-sion The spacial learning and memory are impaired in hypoxia ischemia,which may be related to the de?creasing expression of pCaMKⅡα in neurons in ipsilateral brain.
ABSTRACT
Objective To explore the protective effect of long non-coding RNA(lncRNA) metasta-sis associated in lung denocarcinoma transcript 1 (MALAT1) involved in hyperoxia-induced lung injury in preterm infants.Methods This study had downloaded chip data set GSE25286 (Mouse GEO Genome 430 2.0 Array) from gene expression database gene expression omnibus (GEO),according to the state of hyperoxia exposure,the MALAT1 mRNA expression in rats normal lung tissues and hyperoxic lung tissues was compared at day 14th and 29th.In chip data set GSE43830(Human Exon 1.0 ST Arrays) from GEO,the expression of multi-ple genes[cell division cycle 6(CDC6),death effector domain containing 2(DEDD2),and Cyclin B1 (CCNB1)] in WI38 cells(lung fibroblasts) was compared before and after MALAT1 was knockout.At the same time,the peripheral blood samples of premature infants were collected to verify.Totally 40 premature infants were hospitalized in the department of neonatology in our hospital from Jan 2015 to Dec 2016,the pe-ripheral blood samples of 40 premature infants were collected.RNA was extracted and Real time-PCR was performed after reverse transcription,clinical data of these 40 cases were retrospectively analyzed. Results (1) By using Affymetrix Expression console and Affymetrix Transcriptome analysis console software source files of the chip of pretreatment and difference expression gene screening,the expression of lncRNA MALAT1 gene in lung tissues of hyperoxia lung injury mice significantly upregulated[fold change(FC) =2.33,P=0.001].(2) After MALAT1 in WI38 cell was knockout,MALAT1 expression was significantly reduced(FC= -15.6,P=0.000),the expression of CDC6(FC= -2.37,P=0.001) and CCNB1(FC=-2.16,P=0.002) were down regulated,DEDD2 expression was up regulated(FC =2.46,P =0.000). (3) The results of peripheral blood samples from preterm infants showed that the expression of MALAT1 was significantly increased in preterm infants with hyperoxia-induced lung injury(0.375 5 ± 0.081 9,t =4.634, P=0.015),compared with normal preterm infants(0.273 4 ± 0.067 3).Conclusion Through inhibiting cell apoptosis,lncRNA MALAT1 can protect preterm infants with hyperoxia-induced lung injury,it may provide a new strategy for prevention and treatment of hyperoxia-induced lung injury in premature infants.
ABSTRACT
ObjectiveTo investigate the clinical value of right lateral position with real-time monitor for capsule endoscopy.MethodsA total of 80 patients were randomly divided into two groups.The observation group assumed the right lateral position,while the control group was in upright,standing or sitting position.The capsule endoscope was monitored real time.The patients were allowed to move after the capsule endoscope passed pylorus.Gastric transit time,small bowel transit time,small bowel examination completion rate and positive detection rate were compared between the two groups.ResultsThe mean gastric transit time of the observation group was (31.7 ± 29.8)min,which was significantly shorter than that in the control group (62.6 ± 55.9) min ( U =559.000,P =0.020).The mean transit time of small bowel was (221.3 ±78.8) min in the observation group,which was not significantly different from that of the control group ( t =0.511,P =0.611 ).The examination completion rate of whole small bowel was 95.0％ (38/40)in the observation group,which was significantly higher than that of the control group (x2 =5.165,P =0.023).The positive detection rates were 75.0％ (30/40) and 65.0％ (26/40),respectively,which were not significantly different (x2 =0.952,P =0.329).ConclusionThe right lateral position with real-time monitor during capsule endoscopy is of better clinical value.