Article(id=1207394344991040250, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1207394339840431074, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2022.10.0976, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1643040000000, receivedDateStr=2022-01-25, revisedDate=null, revisedDateStr=null, acceptedDate=1650038400000, acceptedDateStr=2022-04-16, onlineDate=1765794844148, onlineDateStr=2025-12-15, pubDate=1666886400000, pubDateStr=2022-10-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1765794844148, onlineIssueDateStr=2025-12-15, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1765794844148, creator=13701087609, updateTime=1765794844148, updator=13701087609, issue=Issue{id=1207394339840431074, tenantId=1146029695717560320, journalId=1189873630562394117, year='2022', volume='47', issue='10', pageStart='957', pageEnd='1062', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1765794842920, creator=13701087609, updateTime=1765794898634, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1207394573588992611, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1207394339840431074, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1207394573588992612, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1207394339840431074, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=976, endPage=983, ext={EN=ArticleExt(id=1207394346077364999, articleId=1207394344991040250, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Effects of
Lactobacillus acidophilus LA-GHB1756 on alleviating inflammatory bowel disease in mice caused by aspirin, columnId=1190310110212751762, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Basic Research, runingTitle=null, highlight=null, articleAbstract=
Objective Use aspirin to induce mouse inflammatory bowel disease model, and investigate whether Lactobacillus acidophilus LA-GHB1756 can alleviate this type of enteritis injury. Methods A total of 40 male BALB/c mice (6-8 weeks old) was randomized into four groups: control group, aspirin group, LA low-dose group, and LA high-dose group. Except for the control group, the remaining groups were given 0.5 mg/(100 g·d) aspirin solution by gavage for eight weeks to induce inflammatory bowel disease. The LA low-dose and high-dose groups received an additional 2000 cfu/(100 g·d) and 10 000 cfu/(100 g·d) of LA-GHB1756 bacterial liquid, respectively. Accordingly, the control and aspirin groups received the same volume of normal saline through gavage. We then monitored the mouse's body weight, defecation status, hair color, and other conventional indicators, colon macroscopic and pathological staining. We used ELISA to detect intestinal tissue MPO content, serum tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) expression. We employed Western blotting to detect intestinal tissue NF-κB p65 expression levels. Results The general observation of mice in each group showed that LA-GHB1756 could improve the diarrhea, hair, and mental status of aspirin-induced mice. In the 8th week, the body weight of mice in the aspirin group was (21.6±0.5) g. The body weight was statistically significantly improved in the LA low-dose and high-dose groups, which were (22.8±0.4) g and (23.1±0.3) g, respectively (P<0.05). The colon morphology and pathological results showed that LA-GHB1756 could alleviate intestinal mucosal edema and inflammation caused by aspirin in mice. The colon length of mice in the aspirin group was(5.80±0.43) cm, and the colon length of low-dose and high-dose LA groups was (6.17±0.15) cm and (6.50±0.26) cm, respectively. This length improvement was statistically significant (P<0.05). The results of MPO content in intestinal tissues showed that aspirin group was (95.90±11.34) pg/mg, the MPO content in LA low-dose group and LA high-dose group were (76.03±8.72) pg/mg and (51.40±9.12) pg/mg respectively, which was significantly decreased compared with aspirin group, the difference was statistically significant (P<0.05). The results of serum TNF-α and IL-6 expression showed that the concentrations of TNF-α and IL-6 in aspirin group were (238.75±17.80) pg/mg and (292.00±15.51) pg/mg, respectively, while those in LA low-dose group were (207.75±12.04) pg/mg and (250.25±11.50) pg/mg, respectively, LA high-dose group were (80.25±10.24) pg/mg and (108.50±13.38) pg/mg, respectively. Compared with aspirin group, TNF-α and IL-6 contents in LA low-dose group and LA high-dose group were statistically significantly decreased (P<0.05). The expression of NF-κB p65 was increased up to 5.07 fold in aspirin group when compared with control group. This level was statistically significantly decreased to 83.74% and 82.95% in LA low-dose and high-dose groups, respectively (P<0.05). Conclusion LA-GHB1756 can relieve intestinal inflammation in mice caused by aspirin, this effect may be related to the inhibition of MPO and NF-κB p65 expression in intestinal tissue.
, correspAuthors=Hai-Bin Guan, authorNote=null, correspAuthorsNote=
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目的 探讨嗜酸乳杆菌LA-GHB1756对阿司匹林引起的小鼠肠道炎症的影响。方法 将40只6~8周龄BALB/c雄性小鼠分为空白对照组、阿司匹林组、LA低剂量组、LA高剂量组等4组。除空白对照组外,其余各组小鼠给予0.5 mg/(100 g·d)的阿司匹林溶液连续灌胃8周引起肠黏膜损伤;LA低剂量组及LA高剂量组在给予阿司匹林的同时给予LA-GHB1756菌液灌胃,LA低剂量组的剂量为2000 cfu/(100 g·d),LA高剂量组的剂量为10 000 cfu/(100 g·d),空白对照组及阿司匹林组给予同等体积的生理盐水灌胃。观察各组小鼠的体重、排便情况、毛发色泽等常规指标;测量小鼠结肠长度,观察结肠形态并行病理学观察;ELISA法检测肠组织髓过氧化物酶(MPO)含量、血清肿瘤坏死因子-α(TNF-α)及白细胞介素-6(IL-6)浓度;Western blotting检测肠组织核因子(NF)-κB p65的表达量。结果 一般情况观察显示,LA-GHB1756可改善阿司匹林引起的小鼠腹泻及毛发、精神状况改变。在第8周时,阿司匹林组小鼠体重为(21.6±0.5) g,LA低剂量和高剂量组体重明显升高,分别为(22.8±0.4) g和(23.1±0.3) g,差异有统计学意义(P<0.05)。各组小鼠结肠形态及病理学检查结果显示,LA-GHB1756可缓解阿司匹林引起的小鼠肠黏膜水肿及炎症反应,阿司匹林组小鼠结肠长度为(5.80±0.43) cm,LA低剂量和高剂量组小鼠结肠长度分别为(6.17±0.15) cm和(6.50±0.26) cm,均明显长于阿司匹林组,差异有统计学意义(P<0.05)。阿司匹林组小鼠肠组织MPO含量为(95.90±11.34) pg/mg,LA低剂量组及LA高剂量组分别为(76.03±8.72) pg/mg和(51.40±9.12) pg/mg,均低于阿司匹林组,差异有统计学意义(P<0.05)。阿司匹林组小鼠血清TNF-α和IL-6浓度分别为(238.75±17.80) pg/mg和(292.00±15.51) pg/mg,LA低剂量组分别为(207.75±12.04) pg/mg和(250.25±11.50) pg/mg,LA高剂量组分别为(80.25±10.24) pg/mg和(108.50±13.38) pg/mg,均低于阿司匹林组,差异有统计学意义(P<0.05)。阿司匹林组肠组织NF-κB p65表达量是对照组的5.07倍,LA低剂量组及LA高剂量组肠组织NF-κB p65的表达量明显降低,分别降至阿司匹林组的83.74%和82.95%,差异有统计学意义(P<0.05)。结论 嗜酸乳杆菌LA-GHB1756可缓解由阿司匹林引起的小鼠肠道炎症,该作用可能与其抑制肠组织MPO、NF-κB p65的表达相关。
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张丽娟,医学硕士,主治医师,主要从事肠道内分泌疾病方面的研究
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各组小鼠体重变化情况与对照组比较,(1)P<0.05;与阿司匹林组比较,(2)P<0.05
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各组小鼠结肠形态(A)、长度(B)及病理学变化(C)与对照组比较,(1)P<0.05;与阿司匹林组比较,(2)P<0.05
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Comparison of MPO content in intestinal tissue (A) and TNF-α and IL-6 expression in serum (B) of mice in each group, figureFileSmall=Y/Rdj1Yl5GKS3dH9nunRQg==, figureFileBig=6XRzlyZAVfX5w30tsd5xYw==, tableContent=null), ArticleFig(id=1207394352834388008, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1207394344991040250, language=CN, label=图3, caption=
各组小鼠肠组织MPO含量(A)及血清TNF-α和IL-6浓度(B)比较与对照组比较,(1)P<0.05;与阿司匹林组比较,(2)P<0.05
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各组小鼠肠组织NF-κB p65表达量比较与对照组比较,(1)P<0.05;与阿司匹林组比较,(2)P<0.05
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