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2.8延缓果实衰老果实成熟和衰老是果实发育的最后阶段,该阶段直接关系到品质形成和贮藏保鲜。乙烯是一种气态植物激素,是决定果实成熟、衰老和贮藏期的关键因素。在乙烯合成途径中,1-氨基环丙烷-1-羧酸（ACC）是乙烯合成的前体,ACC合成酶（ACS）,即乙烯合成酶（EFE）和ACC氧化酶（ACO）是控制乙烯合成的两种关键酶,二者在跃变型果实成熟衰老进程中均被诱导,并诱发乙烯自我催化大量合成乙烯（乙烯跃变）。 相似文献
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为进一步了解扩展蛋白（Expansin,EXP）在柿果实采后软化过程中的作用,以丙烯和1–甲基环丙烯（1-methylcyclopropene,1-MCP）处理‘富平尖柿’采后果实,采用实时荧光定量PCR技术检测果实中EXP基因表达量的变化。结果显示,丙烯促进柿果实成熟软化,使乙烯释放高峰升高并提前到来,提高ACC合成酶（ACS）、ACC氧化酶（ACO）活性;1-MCP减缓柿果实的成熟软化,推迟并降低乙烯释放高峰,抑制ACS和ACO活性。随着贮藏时间的延长,柿果实逐渐软化,对照果实DkEXP3和DkEXP4的相对表达量均表现为先上升后下降的趋势。丙烯处理促进了DkEXP3和DkEXP4的表达,使表达高峰升高且提早到来;1-MCP处理抑制了DkEXP3和DkEXP4的表达,推迟且降低了表达高峰。对照和1-MCP处理的果实的DkEXP3和DkEXP4的相对表达量高峰均较乙烯释放高峰早。DkEXP3和DkEXP4在果皮、果肉、果心中表达水平不同。本结果说明EXP可能在采后柿果实成熟软化前期起作用,其表达有组织特异性,且受到乙烯的调控。 相似文献
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为了进一步探索木葡聚糖内糖基转移/水解酶（XTH）在柿（Diospyros kaki L.）采后软化中的分子调控机制,应用实时荧光定量PCR 技术检测常温下丙烯和1–甲基环丙烯（1-MCP）处理的‘富平尖柿’果实中XTH 基因表达量的变化。结果显示,丙烯处理能够促进柿果实成熟软化,增加乙烯释放并使高峰提前到来,而1-MCP 处理能够延缓果实软化,抑制乙烯释放。随着柿果实成熟软化推进,4 个XTH 基因呈现不同的表达方式,且丙烯处理促进了4 个XTH 基因的表达,而1-MCP 处理则抑制它们的表达。其中,DkXTH1 和DkXTH2 在柿果实成熟软化过程中表达量较高,且二者表达高峰分别在果实成熟的初期和中期,说明DkXTH1 和DkXTH2 分别与采后柿果实初期和中后期的软化关系密切。结合乙烯释放量结果分析显示,柿果实XTH 基因的表达受乙烯调控,对柿果实的成熟软化中具有一定的促进作用。 相似文献
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钙在乙烯促进网纹甜瓜果实软化过程中的作用 总被引：2，自引：0，他引：2
以网纹甜瓜为试材, 通过测定果实硬度、呼吸速率、乙烯释放量、1-氨基环丙烷基羧酸(ACC) 含量及ACC合成酶(ACS) 和ACC氧化酶(ACO) 的活性, 研究钙在乙烯促进网纹甜瓜果实软化过程中的调控作用。结果表明: 采用浓度为015%外源硝酸钙处理1 h和10μL·L-1外源乙烯处理24 h, 乙烯处理可提高网纹甜瓜果实中水溶性钙含量, 降低果胶酸钙的含量, 提高果实的呼吸速率, 缩短呼吸跃变高峰出现的时间, 并通过提高ACC含量以及ACS和ACO活性, 提高了乙烯释放量; 先乙烯处理后增施钙可进一步提高水溶性钙含量并降低果胶酸钙的含量和提高呼吸速率、ACC含量、ACS和ACO活性以及乙烯释放量。但单施钙可明显提高果实中果胶酸钙的含量, 推迟降低了呼吸速率, 推迟ACC含量、ACS和ACO活性峰值出现的时间及峰度值, 从而降低了果实的乙烯释放量; 而与单用钙处理相比, 先钙后乙烯处理在一定程度上提高了呼吸速率、ACO活性和乙烯释放量, 但是以上各指标仍低于对照。由此可见, 钙虽然具有延缓网纹甜瓜果实软化的作用, 但可促进乙烯诱导条件下网纹甜瓜果实的软化。 相似文献
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香蕉属于呼吸跃变型水果,ACC合成酶(ACS)是乙烯合成路径中的关键限速酶。为了明确调控香蕉果实成熟关键ACS基因,对采后香蕉果实用乙烯利、1-MCP和自然成熟等处理,并利用实时荧光定量PCR分析ACS基因家族成员在果实成熟过程中的表达情况。结果表明,不同家族成员在3种处理中的表达趋势及表达量不一致,3个处理的MaACS4表达趋势一致,均为前期变化不大,成熟时快速增加,但最终上调倍数小于10。乙烯利和1-MCP处理的MaACS6表达量先下降后增加,自然成熟的先增加后下降。3个处理的MaACS10表达量在前期比较低且变化不大,但在成熟时急剧增加并达到峰值,最终上调倍数约1 700倍。乙烯利和1-MCP处理的MaACS13表达量先下降后增加再下降,自然成熟的前期变化不大,但成熟时显著下降。推测MaACS10是调控香蕉成熟的关键基因。 相似文献
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一氧化氮对番茄果实采后成熟和Le-ETR4基因表达的影响 总被引：2，自引：0，他引：2
以破色期的‘卡罗’番茄果实为试材,研究了NO供体硝普钠（SNP）50 μmol · L-1处理30 min对番茄果实采后成熟的作用,并采用Northern杂交技术检测NO对番茄乙烯受体基因Le-ETR4表达的影响。结果表明,50 μmol · L-1 SNP处理降低了番茄果实的乙烯释放速率,抑制了ACC氧化酶（ACC oxidase,ACO）、纤维素酶（Cellulase）和多聚半乳糖醛酸酶（Polygalacturonase,PG）的活性,延缓了果实的色泽变化和软化,同时显著抑制了番茄乙烯受体基因Le-ETR4的表达。以上结果说明NO主要通过抑制番茄乙烯的生物合成和乙烯受体基因表达来控制成熟相关酶的活性,NO可以在生理水平和乙烯受体水平调控番茄果实的成熟。 相似文献
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以‘泰山早霞’苹果成熟的果实为试材,于采收当天进行1–甲基环丙烯（1-MCP）处理,研究其对果实软化及相关基因表达的影响。结果表明,①1-MCP处理的果实在短期贮藏期间硬度均明显高于对照。②1-MCP处理后,乙烯释放速率、PG、PME、β-Gal、α-L-Af及LOX等细胞壁酶基因的表达均被明显抑制,在整个试验期内均有明显下降,尤其是在处理后1 d,就分别比各自的对照下降了72.0%、72.1%、87.5%、81.8%、90.2%和16.7%,而1-MCP对AM和XET基因的表达没有明显作用。上述结果表明,苹果‘泰山早霞’品种属乙烯极敏感型,1-MCP对于延缓其果实软化具有明显作用,其果实软化可能是PG、PME、β-Gal、α-L-Af及LOX等多种基因协同作用的结果。 相似文献
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脱落酸对桃果实成熟软化和乙烯生物合成的影响 总被引：1，自引：0，他引：1
以"白丽"桃为试材,分析了果实室温条件下贮藏过程中外源ABA(脱落酸)处理和NDGA(去甲二氢化愈创木酸,ABA生物合成抑制剂)处理后多聚半乳糖醛酸酶、果胶甲酯酶、ACC合成酶和ACC氧化酶含量的变化,探讨了在室温贮藏条件下ABA对果实成熟软化和乙烯生物合成的影响。结果表明:外源ABA处理可以提高多聚半乳糖醛酸酶和果胶甲酯酶的活性,加速果实硬度软化进程。外源ABA处理可以提高ACC合成酶和ACC氧化酶的活性,使果实乙烯释放量增加并且乙烯释放高峰提前出现。而NDGA处理则可以抑制多聚半乳糖醛酸酶的活性,果胶甲酯酶活性与清水相比虽然有降低,但抑制效果不显著。NDGA对果实硬度下降也有延缓作用。NDGA可以抑制ACC合成酶和ACC氧化酶的活性,从而降低乙烯释放量并且使乙烯释放高峰延时出现。 相似文献
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AIM: To investigate the alteration of classical protein kinase C-α(cPKC-α)in the ascitic white blood cells of rats with acute pancreatitis (AP), and explore the effects of aspirin (ASP) or tetrandrine (Tet) on them. METHODS: The total of 56 health SD rats were divided into four groups, AP+ASP group, AP+Tet group, AP+normal saline (NS) group, and sham operation control (SO) group. AP model was induced by a retrograde injection of 3% sodium deoxycholate into the pancreatic duct. The AP+Tet group received a intraperitoneal injection of Tet (80 mg/kg), respectively. The AP+ASP group received an infusion of ASP (12.5 mg/100 g) by use of a nose-gastric catheter. At 1 h, 5 h after the treatment, cPKC-α in the ascitic white blood cells of AP rats was measured by Western blot and chemiluminescence, and the semi-quantitative values was obtained by Gel-pro analyzer. RESULTS: The values of cPKC-α decreased in AP+NS group, but increased significantly in the groups treated with ASP and Tet (P＜0.05, or P＜0.01). The levels of AMY increased in AP+NS group and decreased in the treated groups significantly (P＜0.05, or P＜0.01). The morphological lesions in the pancreas were attenuated by these medicines. CONCLUSIONS: 1. ASP and Tet increase cPKC-α levels in the ascitic white blood cells of rats with acute pancreatitis. 2. ASP and Tet have protective effects on the morphology and function of the pancreas in the course of AP. 相似文献
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SUN Wei-hao CAO Da-zhong YU Qian OU Xi-long SHEN Hong YU Ting ZHU Feng SUN Yun-liang FU Xi-ling 《园艺学报》2005,21(2):271-275
AIM: To clarify the effects of gastrin on the expression of cyclooxygenase (COX) and several growth factors in rat gastric mucosa. METHODS: Male Sprague Dawley rats were fasted for 24 hours and subcutaneously injected with saline or gastrin 17 at doses of 1 μg/kg, 10 μg/kg and 100 μg/kg, respectively. The expression of COX-1, COX-2, heparin-binding epidermal growth factor-like growth factor (HB-EGF) and hepatocyte growth factor (HGF) in the gastric mucosa were examined using Western blotting and immunohistochemical staining. Effects of a potent gastrin receptor antagonist YM022 on the expression of COX-1, COX-2, HB-EGF and HGF in gastric mucosa were also evaluated. RESULTS: Gastrin dose-dependently increased the expression of COX-2 and HB-EGF in rat gastric mucosa while the expression of COX-1 and HGF did not change significantly after treatment with gastrin. However, pretreatment with YM022 dose-dependently abolished the up-regulation of COX-2 and HB-EGF expression induced by gastrin. CONCLUSIONS: This study demonstrates that gastrin up-regulates COX-2 and HB-EGF expression in rat gastric mucosa, indicating that COX-2 and HB-EGF are involved in pathogenesis of the gastrin-related gastric mucosal hyperplasia and carcinoma of stomach. 相似文献
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AIM:To explore the expression and potential impacts of chaperonin 60 (Cpn60) in the hepatic and pancreatic tissues from animals endured experimental acute pancreatitis (AP) with various severities. METHODS:Induction of mild acute pancreatitis (MAP) in mice was made by intraperitoneal injection of caerulein, and sodium deoxycholate was used by injection through pancreato-biliary duct backward to induce severe acute pancreatitis (SAP) in rats. The liver and pancreas from sacrificed animals at 1 h, 5 h and 10 h time points post-induction of AP were harvested for pathological examination and observing the dynamic change of Cpn60 expression with techniques of immunoprecipitation (IP) and Western blotting. RESULTS:In the MAP and SAP models, pancreatic tissues showed swollen or hemorrhagic necrotic changes, respectively. The characteristic differences of Cpn60 expression were also observed. The Cpn60 protein was expressed as two distinctive bands in pancreatic and hepatic tissues, and relative densities of the two bands varied differently at these time points in both AP models. CONCLUSION:The results suggest that not only the quantitative, but also, probably, qualitative abnormalities of Cpn60 expression in AP exist. These abnormalities may play important roles in the pathogenesis and development of acute pancreatitis. 相似文献
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AIM: To investigate the change of Cpn60 content, the alterations of pancreatic enzymes and lysosome, in order to better understand the mechanism of intrapancreatic enzyme activation in acute pancreatitis(AP). METHODS: The AP model was replicated by retrograde infusion of 4% sodium-deoxycholate in the choledocus of SD rats. The levels of amylase in plasma and TNF-α in pancreatic tissue were measured by biochemical technique at 5 h and 10 h after AP induction. The content of Cpn60 and pancreatic enzymes in different compartments of the acinar cells were tested by quantitative protein A-gold immunocytochemistry technique. The change of lysosome in the acinar cells was observed under the electronic microscope. RESULTS: After AP was induced, the levels of amylase in the plasma and TNF-α in the pancreatic tissue increased significantly. Lysosomes with different forms were found inside the acinar cells, and some of them located in the Golgi apparatus. Cpn60 content decreased, which was accompanied by an increase of lipase or chymotrypsinogen content in the pancreatic secretory pathway. CONCLUSION:In the pancreatic acinarcells of AP rats,Cpn60 content decreased,suggesting an insufficient chaperone capacity,and combining with the change of lysosome both in its amount and locat ion,which may take part in the intrapancreatic enzyme activation and the development of AP. 相似文献
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AIM: To evaluate the effect of isinglass on chronic atrophic gastritis(CAG) in rats and its mechanism. METHODS: An animal model of CAG in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol/L sodium deoxycholate and 0.1% ammonia water was established in SD rats. Isinglass was used as preventive therapy while we were establishing CAG rat model. Finally all the rats were executed and pathologic changes of the gastric mucosa were studied by gross appearance and microscopy and serum epidermal growth factor (EFG) and growth hormone(GH) contents were tested. RESULTS: In each isinglass prevention group, inflammation grade of gastric antrum was less than that in model group (P<0.01) while the mean ratio of the thickness of gastric mucosal gland and muscularis mucosa (L1/L2), the number of gastric glands in 1 mm lengths of mucosal layer in longitudinal sections were much better than those in model group (P<0.01).They were very close to normal control group (P>0.05). The expression of proliferating cell nuclear antigen (PCNA) in gastric mucosa and serum EFG level were higher than those in model group (P<0.01, P<0.05), but serum GH content showed no different between isinglass prevention group and model group. CONCLUSION: Isinglass preventes the gastric mucosal atrophy in the CAG model. Its mechanism may be related to the effects of decreasing the gastric mucosal damage， promoting the cell proliferation and increasing of internal EFG secretion. 相似文献
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Although we have understood only limited knowledge about the pathophysiological mechanisms of acute pancreatitis (AP), it has at least been proven that the activation of pancreatic zymogens inside the pancreatic acinar cells, as well as the inflammatory reaction resulting from the inflammatory mediators, including the cytokines and oxygen free radicals, constitute the main reason for the early pathological processes of AP. The inflammatory mediators also facilitate the complications such as lung injury and multiple organ dysfunctions. The bacterial translocation, which aggravates the pathological changes and increases the mortality in AP, causes the pathophysiological vicious circle in the later period of the disease. There is no doubt that the levels of the clinical prevention, diagnosis and treatment for AP will be greatly improved along with the elucidation of its pathogenesis. 相似文献
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AIM: To observe the dynamic changes of neurokinin A (NKA) and calcitonin gene-related peptide (CGRP) levels in gastric mucosal and plasma in rats after abdominal seawater-immersing trauma, and to investigate the influence of these two sensory neuropeptides on acute gastric mucosal lesion. METHODS: Thirty-two SD rats were randomly divided into four groups (normal group, celiac seawater-immersing trauma 1, 2 and 3 h groups). With emzyoimmunoassay and radioimmunoassay respectively, gastric mucosal and plasma NKA and CGRP levels in rats were measured.RESULTS: Compared with normal rats, with the seawater-immersing time prolonged, gastric mucosal NKA and CGRP levels in rats were progressively decreased (P<0.05), while plasma NKA and CGRP levels significantly elevated. CONCLUSION: Seawater-immersion is a harmful factor, it can lead to elevated plasma NKA and CGRP levels and decrease gastric mucosal NKA and CGRP levels. 相似文献
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AIM:To investigate the expression of inhibitor kappa B alpha (IκBα) in pancreas and liver tissues of rats with experimental acute pancreatitis (AP) and to explore the therapeutic mechanism of Chinese medicine new Qing Yi Tang (QYT) on AP. METHODS:70 SD rats were randomly divided into three groups:normal control group (n=10), AP+QYT group (n=30), and AP+normal saline (NS) group (n=30). AP model was induced by retrograded injection of 4% sodium deoxycholate into the pancreatic duct. QYT or NS was infused to the rats respectively by a gastric catheter repeatedly every five hours after AP induction. At 1 h, 4 h, 10 h after operation, rats were sacrificed, and the pancreas and liver were moved out individually. Real-time RT-PCR was performed to detect IκBα mRNA expression in the liver. Western blotting was applied to detect IκBα protein expression in the liver and pancreas. IκBα proteins including phosphorylated form (IκBα-p) and non-phosphorylated form (IκBα-n) were tested. Serum level of leukotriene C4 (LTC4) was detected by ELISA. The pathological changes of pancreas and lung tissues stained with HE were observed under light microscope. RESULTS:Compared with the normal control group, expression of IκBα mRNA in liver was higher in AP rats in the observation period (P<0.01, or P<0.05). QYT treated group had lower expression of IκBα mRNA as compared with AP+NS group (P<0.05). Expression of IκBα protein (including IκBα-p and IκBα-n) in liver and pancreas were also higher in AP group as compared with that in control group (P<0.05). IκBα-p displayed an increased tendency during the observation period in AP+ NS group. However, QYT treatment induced a decrease in IκBα-p protein expression and an increase in IκBα-n expression. The serum LTC4 level in AP group was increased in a time-dependent manner, and QYT attenuated the increased LTC4 level in certain degree (P<0.05). The pathological changes in pancreas and lung tissues of AP rats, such as edema, hemorrhage, and inflammatory cell infiltration were lightly attenuated by QYT. CONCLUSION:QYT alleviated the inflammatory reaction of AP by inhibiting IκBα-p expression and then reducing the inflammatory mediators. 相似文献
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AIM:To investigate the susceptibility to pancreatitis in LPL deficient hypertriglyceridemic (HTG) mice and to establish an experimental animal model for study on HTG pancreatitis. METHODS:LPL deficient HTG mice was rescued by somatic gene transfer. Plasma amylase and pathological changes in pancreas were analyzed for comparison between LPL deficient HTG and wild type mice to assess the incidence of spontaneous pancreatitis. In addition, acute pancreatitis(AP) was induced by L-arginine for further assessment. RESULTS:According to pancreatic pathological scores, incidence of spontaneous pancreatitis was 34.5% in LPL deficient mice. The affected LPL deficient HTG mice showed typical morphological changes of pancreatitis with inflammatory infiltration and acinar necrosis, accompanying fibrosis or hemorrhage occasionally, while there was no pancreatitis in wild type mice. The severity of pathological changes correlated positively with plasma TG levels （r=0.604，P<0.05）. However, the amylase levels did not increase significantly. When AP inducer, L-arginine, was injected at low dose (2 g/kg body weight, ip), LPL deficient mice showed more severe pathological damage than wild type mice （P<0.01）, though there was no significant change in amylase levels. CONCLUSION:LPL deficient HTG mice developed spontaneous pancreatitis, and the susceptibility to L-arginine-induced pancreatitis increased. These findings show that HTG results in pancreatitis on mice as on human. Therefore, LPL deficient HTG mice would be a useful experimental model for study of HTG pancreatitis. 相似文献
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AIM: To observe the expression and interrelationship of apoptosis controlling genes and proteins Fas, FasL, caspase-3 in rats with acute pancreatitis (AP). METHODS: Forty male Sprague Dawley rats were randomly divided into four groups, 10 rats each group. Acute pancreatitis with different inflammatory degree was induced by retroinjecting 2.0%, 3.5% or 5.0% sodium taurocholate at dose of 1 mL/kg body weight into the pancreaticobiliary duct. All the rats were sacrificed 6 h after operation. The pathologic changes of pancreas were observed under optical microscope. The protein and mRNA expressions of Fas, FasL, caspase-3 in pancreatic tissue were measured by Western blotting and RT-PCR. The apoptosis of acinar cells was measured by the methods of in situ end labeling. RESULTS: In normal pancreatic tissue, there appeared the protein and mRNA expression of Fas, FasL, caspase-3. In acute pancreatitis with different inflammatory degree, with the degree of inflammation worsen, the apoptosis cells tapered, the expression of above protein and mRNA also descended gradually. Furthermore, the variation tendency of caspase-3 among the four groups was in coincidence with Fas or FasL. CONCLUSION: Fas/FasL -mediated apoptotic pathway participates in the regulation of acinar cell apoptosis in acute pancreatitis. 相似文献