PMID- 29931957
OWN - NLM
STAT- MEDLINE
DCOM- 20181017
LR  - 20181017
IS  - 1000-6834 (Print)
IS  - 1000-6834 (Linking)
VI  - 32
IP  - 4
DP  - 2016 Apr 8
TI  - [The role of sub-transform of macrophages in renal ischemia/reperfusion injury in 
      rats].
PG  - 338-342
LID - 10.13459/j.cnki.cjap.2016.04.014 [doi]
AB  - OBJECTIVE: To investigate the role of sub-transform macrophage in 
      ischemia/reperfusion renal injury in rats, as well as under-lying mechanisms. 
      METHODS: Thirty male Sprague-Dawley rats were randomly divided into 
      ischemia/reperfusion (IRI, n=24, renal artery was occluded for 45 min) group and 
      sham-operation (Sham, n=6) group. The kidneys in IRI group were collected at 0, 
      6, 24 and 72 h after operation (6 rats for each time point). The injury of the 
      kidney was detected with HE staining. Immunohistochemistry staining was performed 
      to evaluate the expression of proliferating cell nuclear antigen (PCNA). 
      Real-time PCR was used to detect the mRNA expression of macrophage migration 
      inhibitory factor (MIF). Moreover, the expression and location of MIF, monocyte 
      chemoattractant protein-1 (MCP-1) and macrophage marker CD68 were examined by 
      immunofluorescence staining. Most importantly, the distribution of macrophage 
      subtypes M1 and M2 was analyzed by flow cytometry. RESULTS: The worst pathologic 
      damage of the renal tissues, as well as infiltration of inflammatory cells, was 
      observed at 24 h after operation in IRI rats, with obvious recovery afterwards. 
      Immunohistochemistry staining showed that the expression of PCNA was 
      significantly increased after the ischemia/reperfusion, peaking at 6 h and 
      reducing at 72 h after operation. Compared with sham group, the levels of MIF at 
      mRNA and protein levels were both significantly increased after the 
      ischemia/reperfusion, while the expression of MCP-1 was peaked at 6 h and 
      decreased afterwards. Moreover, the expression of CD68-positive macrophages were 
      significantly increased in IRI rats, with peaking at 24 h and reducing at 72 h. 
      Furthermore, after 6 h of reperfusion, the percentage of M1 macrophages reached 
      the peak, and thereafter the relative expression of M1 and M2 was reduced and 
      increased, respectively. CONCLUSIONS: In the early phase of ischemia/per-fu sion 
      renal injury, M1 macrophage results in renal damage, and afterwards the M2 
      macrophage is increased and repairs the renal damage by improving the cell 
      proliferation.
FAU - Lin, Cheng-Cheng
AU  - Lin CC
AD  - Wenzhou Key Laboratory of Surgery, the First Affiliated Hospital, Wenzhou Medical 
      University, Wenzhou 325000.
FAU - Lu, Hong
AU  - Lu H
AD  - Department of Laboratory Medicine, the First Affiliated Hospital, Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Wu, Lian-Feng
AU  - Wu LF
AD  - Department of Laboratory Medicine, the First Affiliated Hospital, Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Liang, Yong
AU  - Liang Y
AD  - Wenzhou Key Laboratory of Surgery, the First Affiliated Hospital, Wenzhou Medical 
      University, Wenzhou 325000.
FAU - Chen, Bi-Cheng
AU  - Chen BC
AD  - Wenzhou Key Laboratory of Surgery, the First Affiliated Hospital, Wenzhou Medical 
      University, Wenzhou 325000.
FAU - Bai, Yong-Heng
AU  - Bai YH
AD  - Wenzhou Key Laboratory of Surgery, the First Affiliated Hospital, Wenzhou Medical 
      University, Wenzhou 325000.
LA  - chi
PT  - Journal Article
PL  - China
TA  - Zhongguo Ying Yong Sheng Li Xue Za Zhi
JT  - Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = 
      Chinese journal of applied physiology
JID - 9426407
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation, Myelomonocytic)
RN  - 0 (CD68 protein, rat)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Macrophage Migration-Inhibitory Factors)
RN  - EC 5.3.- (Intramolecular Oxidoreductases)
RN  - EC 5.3.2.1 (Mif protein, rat)
SB  - IM
MH  - Acute Kidney Injury
MH  - Animals
MH  - Antigens, CD/metabolism
MH  - Antigens, Differentiation, Myelomonocytic/metabolism
MH  - Cell Proliferation
MH  - Chemokine CCL2/metabolism
MH  - Intramolecular Oxidoreductases/metabolism
MH  - Kidney/*pathology
MH  - Macrophage Migration-Inhibitory Factors/metabolism
MH  - Macrophages/*cytology
MH  - Male
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - *Reperfusion Injury
OTO - NOTNLM
OT  - injury and recovery
OT  - ischemia/reperfusion
OT  - kidney
OT  - macrophage
EDAT- 2016/04/08 00:00
MHDA- 2016/04/08 00:01
CRDT- 2018/06/23 06:00
PHST- 2018/06/23 06:00 [entrez]
PHST- 2016/04/08 00:00 [pubmed]
PHST- 2016/04/08 00:01 [medline]
AID - 10.13459/j.cnki.cjap.2016.04.014 [doi]
PST - ppublish
SO  - Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2016 Apr 8;32(4):338-342. doi: 
      10.13459/j.cnki.cjap.2016.04.014.