PMID- 28795664
OWN - NLM
STAT- MEDLINE
DCOM- 20190214
LR  - 20190215
IS  - 2095-4352 (Print)
VI  - 29
IP  - 8
DP  - 2017 Aug
TI  - [Roles of MyD88 and TRIF in cardiac dysfunction during sepsis].
PG  - 684-688
LID - 10.3760/cma.j.issn.2095-4352.2017.08.003 [doi]
AB  - OBJECTIVE: To investigate the roles of myeloid differentiation factor 88 (MyD88) 
      and TIR domain-containing adaptor inducing interferon-beta (TRIF) in sepsis-induced 
      myocardial dysfunction, and to analyze whether strain rate (SR) can be early 
      sensitive evaluation for septic heart failure. METHODS: Sixty-four healthy male 
      C57BL/6 mice were divided into four groups by random number table (n = 16 in each 
      group): sham group, cecum ligation and puncture (CLP)-induced sepsis model group, 
      anti-MyD88 group and anti-TRIF group. The anti-MyD88 group and anti-TRIF group 
      were injected with 5 muL/g of anti-MyD88 antibody or anti-TRIF antibody through 
      the tail veins 2 hours before CLP. Eight animals in each group were used to 
      observe the survival of 24 hours, and the other 8 myocardial tissues were 
      harvested for examination. The cardiac function was evaluated by echocardiography 
      before and 6 hours and 12 hours after operation. The mRNA expressions of MyD88, 
      TRIF and inflammatory factors in myocardium were measured by polymerase chain 
      reaction (PCR) at 24 hours after operation, and the degree of neutrophils 
      infiltration was detected by myeloperoxidase (MPO) activity. RESULTS: The number 
      of 24-hour survive in anti-MyD88 group and anti-TRIF group were higher than that 
      in CLP group (number: 4, 3 vs. 2, P = 0.044, P = 0.047). Compared with sham 
      group, the cardiac function was significantly decreased, the mRNA expressions of 
      myocardial tissues MyD88, TRIF, interleukin (IL-1, IL-6) and tumor necrosis 
      factor-alpha (TNF-alpha) were significantly increased, and the infiltration of 
      neutrophils were obvious in CLP group. Compared with CLP group, the left 
      ventricular short axis fractional shortening rate (FS) and SR were significantly 
      increased after 12 hours in anti-MyD88 group and anti-TRIF group [FS: 
      (49.52+/-1.78)%, (49.89+/-1.49)% vs. (41.11+/-1.63)%, SR (s(-1)): 17.63+/-2.16, 
      17.85+/-1.64 vs. 12.55+/-1.84]; the mRNA expressions of MyD88, TRIF and inflammatory 
      factors were significantly decreased [MyD88 mRNA (A value): 0.463+/-0.046, 
      0.505+/-0.048 vs. 0.638+/-0.102, TRIF mRNA (A value): 0.413+/-0.031, 0.410+/-0.021 vs. 
      0.625+/-0.057, IL-1 mRNA (A value): 0.569+/-0.101, 0.570+/-0.091 vs. 0.946+/-0.171, IL-6 
      mRNA (A value): 0.551+/-0.143, 0.431+/-0.157 vs. 0.850+/-0.194, TNF-alpha mRNA (A value): 
      0.471+/-0.082, 0.444+/-0.093 vs. 0.707+/-0.094]; and the infiltration of neutrophils 
      were significantly decreased [MPO (U/L): 62.34+/-2.60, 60.87+/-2.40 vs. 73.83+/-4.90], 
      with statistically significant differences (all P < 0.05). There was no 
      statistical difference in above parameters between the anti-MyD88 group and 
      anti-TRIF group (all P > 0.05). CONCLUSIONS: Blocking MyD88 and TRIF expression 
      play significant and similar roles in protecting cardiac deterioration from 
      sepsis by attenuating cytokine release, reducing neutrophil infiltration. SR can 
      sensitively assess septic cardiac dysfunction.
FAU - Zhu, Yun
AU  - Zhu Y
AD  - Department of Ultrasound Diagnosis, the Second Xiangya Hospital, Central South 
      University, Changsha 410011, Hunan, China (Zhu Y, Zhang M, Ouyang MZ, Zhou D); 
      the College of Traditional Chinese Medicine, Hunan University of Chinese 
      Medicine, Changsha 410208, Hunan, China (Li L). Corresponding author: Zhang Ming, 
      Email: zm7626@126.com.
FAU - Zhang, Ming
AU  - Zhang M
FAU - Ouyang, Minzhi
AU  - Ouyang M
FAU - Zhou, Dan
AU  - Zhou D
FAU - Li, Ling
AU  - Li L
LA  - chi
PT  - Journal Article
PL  - China
TA  - Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
JT  - Zhonghua wei zhong bing ji jiu yi xue
JID - 101604552
RN  - 0 (Adaptor Proteins, Vesicular Transport)
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
SB  - IM
MH  - Adaptor Proteins, Vesicular Transport/*metabolism
MH  - Animals
MH  - Heart Diseases/*etiology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Myeloid Differentiation Factor 88/*metabolism
MH  - Sepsis/*complications
EDAT- 2017/08/11 06:00
MHDA- 2019/02/15 06:00
CRDT- 2017/08/11 06:00
PHST- 2017/08/11 06:00 [entrez]
PHST- 2017/08/11 06:00 [pubmed]
PHST- 2019/02/15 06:00 [medline]
AID - 10.3760/cma.j.issn.2095-4352.2017.08.003 [doi]
PST - ppublish
SO  - Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2017 Aug;29(8):684-688. doi: 
      10.3760/cma.j.issn.2095-4352.2017.08.003.