Article(id=1291706993622938327, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.21.012, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1749744000000, receivedDateStr=2025-06-13, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896546035, onlineDateStr=2026-08-05, pubDate=1763308800000, pubDateStr=2025-11-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896546035, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896546035, creator=13701087609, updateTime=1785896546035, updator=13701087609, issue=Issue{id=1291706987964822180, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='21', pageStart='3001', pageEnd='3150', issueExtLink='null', onlineDate='null', pubDate='1763308800000', pubDateStr='2025-11-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896544684, creator='13701087609', updateTime=1785896721343, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291707729324826977, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291707729324826978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3067, endPage=3074, ext={EN=ArticleExt(id=1291706993836847832, articleId=1291706993622938327, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of losartan inhibits GPR84-mediated M1 polarization of macrophages to alleviate renal injury in sepsis, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the molecular mechanism of losartan in alleviating renal injury in sepsis.
Methods In animal experiment, mice were randomly divided into the sham group, the model group (modeled by cecal ligation and perforation), losartan group (losartan treatment at 15 mg·kg-1 after modeling) and antagonist group [treated with the G protein-coupled receptor 84 (GPR84) antagonist GLPG1205 at 30 mg·kg-1 after modeling], each group contained 10 mice. Enzyme-linked immunosorbent assay (ELISA) experiments were used to detect serum renal injury indicators, and immunohistochemistry was used to detect the protein expressions of GPR84 and cluster of differentiation 86 (CD86) in renal tissues. The expression of cytokines in renal tissues was detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR). In cell experiment, THP-1 cells were randomly divided into control group, induce group (induced to M1-type macrophages), medicine group (inducing +10 μg·mL-1 losartan) and medicine+6-OAU group (induction +10 μg·mL-1 losartan +1 μmol·L-1 GPR84 antagonist 6-OAU), the relative expression levels of GPR84 protein was detected by Western blot assay, the relative expression level of CD86 was detected by immunofluorescence assay, and the expression of cytokines in cells was detected by RT-qPCR.
Results In animal experiments, the levels of blood urea nitrogen (BUN) in mice of the sham group, model group, losartan group and antagonist group were (48.55±4.54), (111.28±5.83), (71.52±4.79) and (79.10±8.12) mmol·L-1, respectively; serum creatinine (SCr) were (13.33±1.58),(64.12±6.91), (30.43±5.80) and (40.09±4.49) μmol·L-1, respectively; the average optical density values of GPR84 were 0.05±0.01, 0.08±0.01, 0.05±0.01 and 0.05±0.01, respectively; the average optical density values of CD86 were 0.03±0, 0.08±0.01, 0.05±0.01, 0.06±0.01, respectively; the relative expression levels of GPR84 mRNA were 1.00±0.13, 2.70±0.23, 1.78±0.15 and 1.12±0.09, respectively; interleukin (IL)-1β mRNA were 1.00±0.14, 1.78±0.24, 1.41±0.13 and 1.50±0.19, respectively; tumor necrosis factor-alpha (TNF-α) mRNA were 1.00±0.10, 1.85±0.12, 1.39±0.10 and 1.56±0.12, respectively; the relative expression levels of inducible nitric oxide synthase (iNOS) mRNA were 1.00±0.14, 3.33±0.23, 1.93±0.16 and 2.30±0.24, respectively. Compared between the model group and the sham group; compared the losartan group or the contagonist group with the model group and compared between the losartan group with antagonist group, the differences of the above-mentioned indicators were statistically significant (P<0.05, P<0.01, P<0.001). In cell experiments, the relative expression levels of GPR84 protein in the control group, induce group, medicine group and medicine+6-OAU group were 0.58±0.06, 0.94±0.11, 0.63±0.07 and 1.45±0.09, respectively; the fluorescence intensities of CD86 were (1 072.36±105.92), (3 209.59±206.38), (1 903.95±172.73) and (2 471.43±273.18) a.u.; the relative expression levels of iNOS mRNA were 1.00±0.11, 3.06±0.23, 1.98±0.27 and 2.85±0.24, respectively, the above-mentioned indicators compared between the control group and the induce group, compared between the medicine group and the induce group, and compared between the medicine+6-OAU group and the medicine group, the differences were all statistically significant (all P<0.001).
Conclusion Losartan can alleviate renal injury in sepsis, which is related to the inhibition of GPR84-mediated M1 polarization of macrophages.
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方法 动物实验部分将小鼠随机分为假手术组、模型组（利用盲肠结扎穿孔术建模）、氯沙坦组（建模后给予15 mg·kg-1的氯沙坦治疗）、拮抗剂组[建模后给予30 mg·kg-1的G蛋白偶联受体84（GPR84）拮抗剂GLPG1205治疗]，每组10只。用酶联免疫吸附（ELISA）实验法检测血清肾损伤指标，用免疫组化法检测肾组织GPR84和分化簇86（CD86）蛋白相对表达水平；用实时荧光定量聚合酶链反应（RT-qPCR）法检测肾组织细胞因子表达。细胞实验部分把THP-1细胞随机分为对照组、诱导组（M1型巨噬细胞诱导）、药物组（诱导+10 μg·mL-1的氯沙坦）、药物+6-OAU组（诱导+10 μg·mL-1的氯沙坦+1 μmol·L-1的GPR84激动剂6-OAU），用蛋白质印迹（Western blot）实验法检测GPR84蛋白相对表达水平，用免疫荧光实验法检测CD86相对表达水平，用RT-qPCR法检测细胞因子相对表达水平。
结果 动物实验部分假手术组、模型组、氯沙坦组和拮抗剂组小鼠的血尿素氮（BUN）水平分别为（48.55±4.54）、（111.28±5.83）、（71.52±4.79）和（79.10±8.12）mmol·L-1；血清肌酸酐（SCr）分别为（13.33±1.58）、（64.12±6.91）、（30.43±5.80）和（40.09±4.49）μmol·L-1；GPR84平均光密度值分别为0.05±0.01、0.08±0.01、0.05±0.01和0.05±0.01,CD86平均光密度值分别为0.03±0、0.08±0.01、0.05±0.01和0.06±0.01；GPR84 mRNA相对表达水平分别为1.00±0.13、2.70±0.23、1.78±0.15和1.12±0.09；IL-1β mRNA相对表达水平分别为1.00±0.14、1.78±0.24、1.41±0.13和1.50±0.19；肿瘤坏死因子-α（TNF-α）mRNA相对表达水平分别为1.00±0.10、1.85±0.12、1.39±0.10和1.56±0.12；诱导型一氧化氮合酶（iNOS）mRNA相对表达水平分别为1.00±0.14、3.33±0.23、1.93±0.16和2.30±0.24，模型组的上述指标与假手术组比较，氯沙坦组和拮抗剂组的上述指标分别与模型组比较，拮抗剂组的上述指标分别与氯沙坦组比较，在统计学上差异均有统计学意义（P<0.05，P<0.01，P<0.001）。细胞实验部分对照组、诱导组、药物组和药物+6-OAU组GPR84蛋白相对表达水平分别为0.58±0.06、0.94±0.11、0.63±0.07和1.45±0.09；CD86荧光强度分别为（1 072.36±105.92）、（3 209.59±206.38）、（1 903.95±172.73）和（2 471.43±273.18）a.u.；iNOS mRNA相对表达水平分别为1.00±0.11、3.06±0.23、1.98±0.27和2.85±0.24；诱导组的上述指标与对照组比较，药物组的上述指标与诱导组比较，药物+6-OAU组的上述指标与药物组比较，在统计学上差异均有统计学意义（均P<0.001）。
结论 氯沙坦可减轻脓毒症肾损伤，这与抑制GPR84介导的巨噬细胞M1极化相关。
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魏思灿（1980-），男，副主任医师，主要从事急危重症医学方面的研究
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