PMID- 34790277
OWN - NLM
STAT- MEDLINE
DCOM- 20220301
LR  - 20220428
IS  - 1875-8630 (Electronic)
IS  - 0278-0240 (Print)
IS  - 0278-0240 (Linking)
VI  - 2021
DP  - 2021
TI  - Aspirin Exerts Neuroprotective Effects by Reversing Lipopolysaccharide-Induced 
      Secondary Brain Injury and Inhibiting Matrix Metalloproteinase-3 Gene Expression.
PG  - 3682034
LID - 10.1155/2021/3682034 [doi]
LID - 3682034
AB  - OBJECTIVE: This study is aimed at exploring the possible neuroprotective 
      mechanism of aspirin and the effect of bacterial endotoxin lipopolysaccharide 
      (LPS) during cerebral ischaemia-reperfusion (CIRP) injury. METHODS: We 
      established three animal models: the CIRP, LPS, and CIRP+LPS models. Mortality, 
      the injured brain area, and the beam walking test were used to estimate the 
      degree of cerebral injury among the rats. Immunohistochemistry and 
      immunofluorescence were used to detect activated microglia, matrix 
      metalloproteinase-3 (MMP-3), and osteopontin (OPN). RESULTS: The injured brain 
      area and mortality were dramatically reduced (p < 0.01), and the beam walking 
      test scores were elevated (p < 0.01) in the acetylsalicylic acid (ASA) group 
      compared to the control group. The number of microglia-, MMP-3-, and OPN-positive 
      cells also increased. Furthermore, the number of GSI-B4, OPN, and MMP-3 cells 
      decreased in the ASA group compared to the control group. After LPS stimulation, 
      the number of microglia reached a peak at 24 h; at 7 d, these cells disappeared. 
      In the ASA group, the number of microglia was significantly smaller (p < 0.05), 
      especially at 24 h (p < 0.01), compared to the LPS group. Moreover, the injured 
      brain area and the mortality were dramatically increased and the beam walking 
      test scores were reduced (p < 0.01) after LPS simulation following CIRP. The 
      degree of injury in the ASA group resembled that in the control group. However, 
      the number of MMP-3-immunoreactive neurons or microglia was significantly larger 
      than that of the control group (p < 0.05). In the ASA group, the MMP-3 expression 
      was also considerably decreased (p < 0.05). CONCLUSIONS: After CIRP, microglia 
      were rapidly activated and the expression of MMP-3 and OPN significantly 
      increased. For rats injected with LPS at reperfusion, the injured brain area and 
      mortality also dramatically increased and the neurologic impairment worsened. 
      However, ASA exhibited a neuroprotective effect during CIRP injury. Furthermore, 
      ASA can reverse LPS-induced cerebral injury and inhibit the inflammatory reaction 
      after CIRP injury.
CI  - Copyright (c) 2021 Depeng Feng et al.
FAU - Feng, Depeng
AU  - Feng D
AD  - Department of Neurology, Liaocheng People's Hospital and Liaocheng Clinical 
      School of Shandong First Medical University, Shandong Province, China.
FAU - Chen, Dezhe
AU  - Chen D
AD  - Department of Neurology, Liaocheng People's Hospital and Liaocheng Clinical 
      School of Shandong First Medical University, Shandong Province, China.
FAU - Chen, Tuanzhi
AU  - Chen T
AUID- ORCID: 0000-0001-8444-4693
AD  - Department of Neurology, Liaocheng People's Hospital and Liaocheng Clinical 
      School of Shandong First Medical University, Shandong Province, China.
FAU - Sun, Xiaoqian
AU  - Sun X
AUID- ORCID: 0000-0002-1356-3887
AD  - Department of Neurology, Liaocheng People's Hospital and Liaocheng Clinical 
      School of Shandong First Medical University, Shandong Province, China.
LA  - eng
PT  - Journal Article
DEP - 20211108
PL  - United States
TA  - Dis Markers
JT  - Disease markers
JID - 8604127
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Neuroprotective Agents)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/pharmacology
MH  - Aspirin/*pharmacology
MH  - Brain Injuries/chemically induced/enzymology/pathology/*prevention & control
MH  - Gene Expression Regulation, Enzymologic/*drug effects
MH  - Lipopolysaccharides/*toxicity
MH  - Macrophages/drug effects/metabolism/pathology
MH  - Male
MH  - Matrix Metalloproteinase 3/*chemistry
MH  - Microglia/drug effects/metabolism/pathology
MH  - Neurons/drug effects/metabolism/pathology
MH  - Neuroprotective Agents/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
PMC - PMC8592756
COIS- We declare no conflict of interests.
EDAT- 2021/11/19 06:00
MHDA- 2022/03/03 06:00
PMCR- 2021/11/08
CRDT- 2021/11/18 06:58
PHST- 2021/09/27 00:00 [received]
PHST- 2021/10/14 00:00 [revised]
PHST- 2021/10/21 00:00 [accepted]
PHST- 2021/11/18 06:58 [entrez]
PHST- 2021/11/19 06:00 [pubmed]
PHST- 2022/03/03 06:00 [medline]
PHST- 2021/11/08 00:00 [pmc-release]
AID - 10.1155/2021/3682034 [doi]
PST - epublish
SO  - Dis Markers. 2021 Nov 8;2021:3682034. doi: 10.1155/2021/3682034. eCollection 
      2021.