PMID- 26805532
OWN - NLM
STAT- MEDLINE
DCOM- 20170313
LR  - 20181202
IS  - 2095-4352 (Print)
VI  - 28
IP  - 1
DP  - 2016 Jan
TI  - [The effect of resveratrol on paraquat-induced acute lung injury in mice and its 
      mechanism].
PG  - 33-7
LID - 10.3760/cma.j.issn.2095-4352.2016.01.007 [doi]
AB  - OBJECTIVE: To investigate the effect of resveratrol (Res) on paraquat 
      (PQ)-induced acute lung injury (ALI) and mortality in mice and the mechanism of 
      nuclear factor-KappaB (NF-KappaB) inflammatory pathway. METHODS: Sixty-eight healthy male 
      ICR mice with grade SPF were enrolled, among them 20 mice were used for mortality 
      observation (n = 10), and other 48 were used for determination of related 
      parameters (n = 6). The mice were randomly divided into four groups: normal 
      saline (NS) control group, Res control group, PQ group and PQ + Res group. The 
      mice in the latter two groups were subdivided into 6, 24, 72 hours subgroups. The 
      PQ poisoning model of mice was reproduced by one injection of 30 mg/kg PQ 
      intraperitoneally. The mice in PQ + Res group were given 60 mg/kg Res 
      intraperitoneally on the contralateral side after PQ injection. The mice were 
      sacrificed at 6, 24, 72 hours after PQ poisoning, and lung tissue was harvested. 
      The serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukins (IL-6 and 
      IL-1beta) were determined by enzyme linked immunosorbent assay (ELISA). The 
      pathological changes in lung tissue were observed with electron microscopy. 
      Apoptosis cells in the lung were identified by terminal dexynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) for the estimation of 
      apoptosis rate. The protein expression of NF-KappaB p65 was determined by Western 
      Blot. RESULTS: Compared with PQ group, the death number of mice at 48, 72, 96 
      hours in PQ + Res group was slightly decreased (0 vs. 2, 2 vs. 5, 4 vs. 6) but 
      without statistically significant difference (all P > 0.05). Under electron 
      microscope, the lung injury in PQ group was severer than that in NS control 
      group, and Res was found to be able to alleviate the lung injury. Compared with 
      NS control group [(2.45+/-0.61)%], the apoptosis rate at 6 hours in PQ group was 
      significantly increased [(8.42+/-1.48)%], and peaked at 72 hours [(21.23+/-3.47)%]. 
      Res could decrease the apoptosis rate after PQ poisoning [6 hours: (5.56+/-1.31)% 
      vs. (8.42+/-1.48)%, 24 hours: (11.14+/-2.07)% vs. (16.88+/-2.96)%, 72 hours: 
      (13.28+/-2.32)% vs. (21.23+/-3.47)%, all P < 0.05]. The serum levels of TNF-alpha, IL-6, 
      and IL-1beta, and NF-KappaB p65 in lung tissue were all markedly increased after PQ 
      poisoning, and they were significantly decreased after Res intervention as 
      compared with those of PQ group [TNF-alpha (ng/L): 2.62+/-0.29 vs. 4.06+/-0.74 at 6 
      hours, 3.98+/-0.41 vs. 6.79+/-0.80 at 24 hours, 5.06+/-0.75 vs. 11.00+/-0.75 at 72 hours; 
      IL-6 (ng/L): 14.19+/-1.54 vs. 16.55+/-1.24 at 6 hours, 13.21+/-1.37 vs. 19.73+/-0.85 at 
      24 hours, 13.72+/-0.56 vs. 22.45+/-0.72 at 72 hours; IL-1beta (ng/L): 8.54+/-1.64 vs. 
      12.59+/-0.66 at 6 hours, 10.15+/-0.29 vs. 16.24+/-1.03 at 24 hours, 16.14+/-0.70 vs. 
      19.55+/-0.56 at 72 hours; 6-hour NF-KappaB p65: (1.34+/-0.07) folds vs. (1.86+/-0.11) folds 
      when the expression in NS control group was represented as 1, all P < 0.05]. 
      CONCLUSIONS: Res cannot lower the mortality in mice with PQ poisoning, but it 
      seems to be able to attenuate PQ-induced ALI and cell apoptosis. The mechanism 
      responsible for the latter maybe the inhibitive effect of Res on NF-KappaB p65 
      translocation and cytokines production.
FAU - Zhao, Guangju
AU  - Zhao G
AD  - Department of Emergency, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, Zhejiang, China. Corresponding author: Lu Zhongqiu, 
      Email: lzq640815@163.com.
FAU - Li, Shengqin
AU  - Li S
FAU - Hong, Guangliang
AU  - Hong G
FAU - Li, Mengfang
AU  - Li M
FAU - Wu, Bin
AU  - Wu B
FAU - Qiu, Qiaomeng
AU  - Qiu Q
FAU - Lu, Zhongqiu
AU  - Lu Z
LA  - chi
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
JT  - Zhonghua wei zhong bing ji jiu yi xue
JID - 101604552
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Stilbenes)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - PLG39H7695 (Paraquat)
RN  - Q369O8926L (Resveratrol)
SB  - IM
MH  - *Acute Lung Injury
MH  - Animals
MH  - Apoptosis
MH  - Interleukin-1beta
MH  - Interleukin-6
MH  - Lung
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - NF-kappa B
MH  - Paraquat
MH  - Resveratrol
MH  - Stilbenes
MH  - Tumor Necrosis Factor-alpha
EDAT- 2016/01/26 06:00
MHDA- 2017/03/14 06:00
CRDT- 2016/01/26 06:00
PHST- 2016/01/26 06:00 [entrez]
PHST- 2016/01/26 06:00 [pubmed]
PHST- 2017/03/14 06:00 [medline]
AID - 10.3760/cma.j.issn.2095-4352.2016.01.007 [doi]
PST - ppublish
SO  - Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2016 Jan;28(1):33-7. doi: 
      10.3760/cma.j.issn.2095-4352.2016.01.007.