Enteral immune-microecological nutrition support suppresses inflammatory response in rats with acute pancreatitis
- Author:
- No author available
- Journal Title:
- Chinese Journal of Biomedical Engineering
- Issue:
- 5
- DOI:
- 10.3760/cma.j.cn115668-20210207-00022
- Key Word:
- 肠内免疫微生态营养;Toll样受体4;髓样分化因子88;急性胰腺炎;炎症反应;Enteral immune microecological nutrition;Toll-like receptor 4;Myeloid differentiation factor 88;Acute pancreatitis;Inflammatory response
Abstract： Objective:To investigate the effect of enteral immune-microecological nutrition (EIN) nutritional support on inflammatory response in rats with acute pancreatitis and its mechanism.Methods:Thirty-two male Sprague Dawley rats were randomly divided into the control group, model group, enteral nutrition (EN) group and EIN group. The model of acute pancreatitis was established in the model group, EN group and EIN group. The control group and model group were not intervened, while the EN group and EIN group were intervened with EN and EIN protocols, respectively. After the intervention, the rats were harvested for pancreatic glands which were then analyzed for pathological characteristics by HE staining. The blood levels of amylase (AMY) , pancrelipase (LPS) , calcium (Ca 2+) , tumor necrosis factor (TNF-α) and Interleukin 1β (IL-1 β) were measured. The mRNA and protein levels of Toll-like receptor 4 (TLR4) , myeloid differentiation factor 88 (MyD88) and β - actin were examined by PCR and Western blotting. Results:In the EIN group, the pancreatic lobule showed destructed structure uder microscopy, with purplish red necrotic foci, interstitial hyperemia and edema, and a small amount of inflammatory cells infiltration in the necrotic area. After intervention, there were significant differences in AMY, LPS, Ca 2+, TNF-α, and IL-1β across the control group, model group, EN group and EIN group. Among them, the Ca 2+ level was lowest in the model group, and was significantly higher in the EIN group compared with the model group and the EN group ( P<0.05) . There were also significant differences in TLR4 and MyD88 mRNA and protein expression across the control group, model group, EN group and EIN group. These expression levels were highest in the model group, and was significantly lower in the EIN group compared with the model group and EN group ( P<0.05) . Conclusion:EIN nutritional support can effectively inhibit the inflammatory response in rats with acute pancreatitis via the TLR4/MyD88 pathway and thereby reduce the expression of inflammatory factors.
- [1]税金凤,余婷媛,许媛,等.埃索美拉唑联合免疫肠内营养治疗对重症急性胰腺炎患者肠黏膜屏障和相关细胞因子的影响[J].2018,(2).
- [2]陈少銮,李俊达.急性胰腺炎患者ET、NO与NLRP3炎性体的相关性探讨[J].2019,(8).
- [3]任辉邦,李海珍,张斌,等.藏茵陈对重症胰腺炎大鼠TLR9/MyD88/NF-κBp65信号通路的影响[J].2020,(7).
- [4]崔海涛,赵红梅.谷氨酰胺联合早期肠内营养对重症急性胰腺炎患者菌群移位及炎症反应的影响[J].2018,(12).
- [5]舒艾娅,符宜龙,简万均,等.血液灌流联合持续性血液净化治疗对重症急性胰腺炎 全身炎症反应综合征患者临床疗效、炎性因子和预后的影响[J].2020,(5).
- [6]黄蕾,赵先林,王明皓,等.腺苷酸活化蛋白激酶在急性胰腺炎中的作用[J].2019,(10).
- [7]Antonio Rodriguez-Nicolas,Pilar Jiménez,F. David Carmona,etc.Association between Genetic Polymorphisms of Inflammatory Response Genes and Acute Pancreatitis[J].2019,48(6).
- [8]Laura Letícia de Freitas Chama,Frank Ulrich Weiß,Elke Krüger,etc.LMP7 immunoproteasome knockout mice show delayed inflammatory response during acute pancreatitis: protective or harmful effect?[J].2018,18(Supplement ).
- [9]Liu Lixin,Zhang Sulin,Wang Yirui,etc.BIG1 controls macrophage pro-inflammatory responses through ARF3-mediated PI(4,5)P2 synthesis[J].2020,11(5).
- [10]杨晨,王鹏飞,牛陆杰,等.肠内免疫微生态营养支持通过JAK2/STAT3途径对急性胰腺炎大鼠炎症反应的作用研究[J].2020,(3).
- [11]Jiang, Xue,Pei, Li-Ying,Guo, Wen-Xiu,etc.Glutamine supported early enteral therapy for severe acute pancreatitis: A systematic review and meta-analysis[J].2020,29(2).
- [12]Marta Serafini,Celia Cordero-Sanchez,Rosanna Di Paola,etc.Store-Operated Calcium Entry as a Therapeutic Target in Acute Pancreatitis: Discovery and Development of Drug-Like SOCE Inhibitors[J].2020,63(23).
- [13]Kong Lei,Wu Qinghua,Zhao Liangchao,etc.Effect of microRNA‐27a‐5p on apoptosis and inflammatory response of pancreatic acinar cells in acute pancreatitis by targeting PTEN[J].2019,120(9).
- [14]Xinyun,Zhu,Lijie,Yang,Xianglei,Li,etc.Efficacy and safety of acupuncture on relieving abdominal pain and distension for acute pancreatitis: A protocol for systematic review.[J].2020,99(8).
- [15]Iqbal, Umair,Makar, Michael,Shah, Ruchit N.,etc.PlasmaLyte Improves Patient Outcomes Compared With Normal Saline in the Treatment of Acute Pancreatitis[J].2020,49(5).
- [16].Intraosseous Medullary Fat Necrosis on Tc-99m-MDP Bone Scan of Patient With Acute Pancreatitis[J].2020,45(6).
- [17].Predictors of underlying pancreatic cancer in patients with acute pancreatitis: a Danish nationwide cohort study[J].2020,22(4).
- [18].Nineteen Cases of Severe Acute Pancreatitis in Pregnancy A 5-Year Single-Center Retrospective Analysis[J].2020,49(6).
- [19]Naigang Wang,Cuiping Geng,Haiyun Sun,etc.Hesperetin ameliorates lipopolysaccharide-induced acute lung injury in mice through regulating the TLR4–MyD88–NF-κB signaling pathway[J].2019,42(12).
- [20]Amiti,Ramasamy,Tamizhselvi,Venkatraman,Manickam.Menadione (vitamin K3) inhibits hydrogen sulfide and substance P via NF-кB pathway in caerulein-induced acute pancreatitis and associated lung injury in mice.[J].2019,19(2).
- [21]Madoka Esaki,Takumi Ishida,Yuu Miyauchi,etc.The effect of dihydropyrazines on lipopolysaccharide-stimulated human hepatoma HepG2 cells via regulating the TLR4-MyD88-mediated NF-κB signaling pathway[J].2020,45(7).