Pub Date : 2012-11-05DOI: 10.4172/scientificreports.457
Wang Wan-tie
Aim: This prospective study aimed at investigating the effect of propofol on the expression of protein kinase C (PKC) mRNA during pulmonary ischemia-reperfusion injury (PIRI) in the rabbits. Methods: Single lung ischemia-reperfusion animal model was administrated in vivo. The rabbits were randomly divided into three groups): sham-operated group (Sham); pulmonary I/R group (PIR) and PIR+propofol group (PIR+PPF). Changes of several parameters, including malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity, nitric oxide (NO) content, wet/dry ratio of lung tissue (W/D) and the index of quantitative assessment of histologic lung injury (IQA) were measured at 60 min after reperfusion. Meanwhile, the location and expression of PKC mRNA were observed, lung tissues were also harvested for histopathological evaluation. Results: As compared with PIR group, PKC mRNA is largely expressed in intima and extima of small pulmonary artery as well as thin-wall vessels (mostly small pulmonary veins). The average optical density values of PKC-α, δ and θ mRNA in small pulmonary veins in PIR+PPF group showed obviously higher than that in group PIR (all P<0.01); the activity of SOD increased, the concentration of MDA, W/D and IQA decreased at 60 min after reperfusion in lung tissue (P<0.01 and P<0.05). Abnormal morphological changes of the lung tissue were lessened markedly in PIR+PPF group. Conclusions: The results of this study suggested that propofol possesses and acts its notable protective effect on PIRI in rabbits by activating PKC-α, δ and θ mRNA expression in lung tissue, raising NO level, reducing OFR level and decreasing lipid peroxidation.
{"title":"Effect of Propofol on Expression of PKC mRNA in Pulmonary Injury Induced by Ischemia-Reperfusion in Rabbits","authors":"Wang Wan-tie","doi":"10.4172/scientificreports.457","DOIUrl":"https://doi.org/10.4172/scientificreports.457","url":null,"abstract":"Aim: This prospective study aimed at investigating the effect of propofol on the expression of protein kinase C (PKC) mRNA during pulmonary ischemia-reperfusion injury (PIRI) in the rabbits. Methods: Single lung ischemia-reperfusion animal model was administrated in vivo. The rabbits were randomly divided into three groups): sham-operated group (Sham); pulmonary I/R group (PIR) and PIR+propofol group (PIR+PPF). Changes of several parameters, including malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity, nitric oxide (NO) content, wet/dry ratio of lung tissue (W/D) and the index of quantitative assessment of histologic lung injury (IQA) were measured at 60 min after reperfusion. Meanwhile, the location and expression of PKC mRNA were observed, lung tissues were also harvested for histopathological evaluation. Results: As compared with PIR group, PKC mRNA is largely expressed in intima and extima of small pulmonary artery as well as thin-wall vessels (mostly small pulmonary veins). The average optical density values of PKC-α, δ and θ mRNA in small pulmonary veins in PIR+PPF group showed obviously higher than that in group PIR (all P<0.01); the activity of SOD increased, the concentration of MDA, W/D and IQA decreased at 60 min after reperfusion in lung tissue (P<0.01 and P<0.05). Abnormal morphological changes of the lung tissue were lessened markedly in PIR+PPF group. Conclusions: The results of this study suggested that propofol possesses and acts its notable protective effect on PIRI in rabbits by activating PKC-α, δ and θ mRNA expression in lung tissue, raising NO level, reducing OFR level and decreasing lipid peroxidation.","PeriodicalId":10222,"journal":{"name":"中国病理生理杂志","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2012-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70339660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-01-01DOI: 10.3724/sp.j.1008.2008.00917
Jin Xian-qiao
AIM:To investigate the effects of Aspergillus fumigatus extract (AFE) on the expressions of Muc5ac in human bronchial epithelial cells and its possible mechanism. METHODS: Human bronchial epithelial cells (16HBE-14o) were cultured in vitro, which were exposed to different concentrations of AFE (0, 8, 16, 20 mg/L) for different times. In order to explore the mechanisms, heat-treated AFE, serine protease inhibitors (aprotinin) and protease-activated receptor-2 (PAR-2) antagonist (FSLLRY-NH2) were used. The production and release of Muc5ac in different intervals were tested by immunohistochemistry and ELISA. The expression of Muc5ac mRNA was measured by RT-PCR. RESULTS: In normal control group, only a few Muc5ac was detected. In the experimental groups with AFE exposure, cells produced more Muc5ac compared to normal control group (P0.01), which were positively related to the exposure time or the concentration of AFE. Aprotinin and PAR-2 antagonist (FSLLRY-NH2) inhibited the effect of AFE on Muc5ac production by 16HBE-14o. Heat-treated AFE, which lost protease activities, exerted no effect on Muc5ac production and mRNA expression. CONCLUSION: AFE, depending on its protease activity, activates PAR-2 and causes airway epithelial cells to produce and release more Muc5ac, which may contribute to deterioration of asthma.
{"title":"Effects of Aspergillus fumigatus extract on expression of Muc5ac in human bronchial epithelial cells","authors":"Jin Xian-qiao","doi":"10.3724/sp.j.1008.2008.00917","DOIUrl":"https://doi.org/10.3724/sp.j.1008.2008.00917","url":null,"abstract":"AIM:To investigate the effects of Aspergillus fumigatus extract (AFE) on the expressions of Muc5ac in human bronchial epithelial cells and its possible mechanism. METHODS: Human bronchial epithelial cells (16HBE-14o) were cultured in vitro, which were exposed to different concentrations of AFE (0, 8, 16, 20 mg/L) for different times. In order to explore the mechanisms, heat-treated AFE, serine protease inhibitors (aprotinin) and protease-activated receptor-2 (PAR-2) antagonist (FSLLRY-NH2) were used. The production and release of Muc5ac in different intervals were tested by immunohistochemistry and ELISA. The expression of Muc5ac mRNA was measured by RT-PCR. RESULTS: In normal control group, only a few Muc5ac was detected. In the experimental groups with AFE exposure, cells produced more Muc5ac compared to normal control group (P0.01), which were positively related to the exposure time or the concentration of AFE. Aprotinin and PAR-2 antagonist (FSLLRY-NH2) inhibited the effect of AFE on Muc5ac production by 16HBE-14o. Heat-treated AFE, which lost protease activities, exerted no effect on Muc5ac production and mRNA expression. CONCLUSION: AFE, depending on its protease activity, activates PAR-2 and causes airway epithelial cells to produce and release more Muc5ac, which may contribute to deterioration of asthma.","PeriodicalId":10222,"journal":{"name":"中国病理生理杂志","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69736908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The phenomenon of RNA interference (RNAi) is highly conserved mechanism in the organism evolution. As a immune system ,RNAi is a ubiquitous mechanism against invading microorganism in plant and animal cells. Recently, it has been found that RNAi is the process by which double-strand RNA(dsRNA) directs sequence-specific degradation of messenger RNA and the mediations of sequence specific messenger RNA degradation are 21-and 23-nucleotide small interfering RNAs that generate by ribonuclease from endogenous longer dsRNA or by transfectious technics from heterologous dsRNA. Over the past few years, the way in which cells respond to dsRNA by silencing homologous genes has revealed a new regulating paradigm in biology.
{"title":"The RNA interference","authors":"Kong Xiangping, Pla Air","doi":"10.5772/60631","DOIUrl":"https://doi.org/10.5772/60631","url":null,"abstract":"The phenomenon of RNA interference (RNAi) is highly conserved mechanism in the organism evolution. As a immune system ,RNAi is a ubiquitous mechanism against invading microorganism in plant and animal cells. Recently, it has been found that RNAi is the process by which double-strand RNA(dsRNA) directs sequence-specific degradation of messenger RNA and the mediations of sequence specific messenger RNA degradation are 21-and 23-nucleotide small interfering RNAs that generate by ribonuclease from endogenous longer dsRNA or by transfectious technics from heterologous dsRNA. Over the past few years, the way in which cells respond to dsRNA by silencing homologous genes has revealed a new regulating paradigm in biology.","PeriodicalId":10222,"journal":{"name":"中国病理生理杂志","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70983695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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