PMID- 36299606
OWN - NLM
STAT- MEDLINE
DCOM- 20221105
LR  - 20221105
IS  - 1942-0994 (Electronic)
IS  - 1942-0900 (Print)
IS  - 1942-0994 (Linking)
VI  - 2022
DP  - 2022
TI  - Exploration of the Protective Mechanism of Bax Removal against Ischemia 
      Reperfusion Injury of Skin Flap through the p38 Mitogen-Activated Protein Kinase 
      Pathway.
PG  - 1175078
LID - 10.1155/2022/1175078 [doi]
LID - 1175078
AB  - This research is aimed at exploring the influences of the Bax gene in the p38 
      mitogen-activated protein kinase (MAPK) pathway and its protective mechanism 
      against ischemia-reperfusion injury (IRI) of skin flap. Forty male Sprague-Dawley 
      (SD) rats were equally divided into the experimental group (Bax gene knockout 
      rats) and control group. The dorsal flap model was prepared, and the survival 
      rate of flap was observed after surgery. The rat flap tissue was cut and stained 
      with hematoxylin-eosin (HE) and in situ terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL). The distribution 
      characteristics of p38MAPK and Bax were detected to evaluate the protective 
      mechanism of Bax gene knockout on IRI of skin flap. After surgery, the survival 
      rate of flaps in the experimental group (82.32%, 70.28%) was significantly higher 
      than that in the control group (57.64%, 46.14%) (P < 0.05). The results of HE 
      staining showed that on the 1(st) day after surgery, compared with those in the 
      control group, the skin flaps of the rats in the experimental group were arranged 
      more neatly. The results of TUNEL staining showed that compared with that of the 
      control group, the tissue structure of the skin flap of the experimental group 
      was normal and only a few apoptotic cells appeared. In addition, compared with 
      that in the control group (7.14, 4.25, 3.48, 2.18/6.46, 7.12, 4.86, and 2.44), 
      the expression of Bax and p38 MAPK in the experimental group (0.96, 0.81, 0.76, 
      0.55/1.63, 1.33, 1.01, and 0.56) significantly decreased (P < 0.05). In short, 
      after the Bax gene was knocked out, injury of the flap after ischemia-reperfusion 
      was considerably improved, which may play a protective role on the IRI of the 
      flap by affecting the p38MAPK pathway.
CI  - Copyright (c) 2022 Yapeng Wang et al.
FAU - Wang, Yapeng
AU  - Wang Y
AD  - Department of Orthopaedics, Wuxi No. 9 People's Hospital Affiliated to Soochow 
      University, Wuxi 214000 Jiangsu, China.
FAU - Wu, Yongwei
AU  - Wu Y
AD  - Department of Orthopaedics, Wuxi No. 9 People's Hospital Affiliated to Soochow 
      University, Wuxi 214000 Jiangsu, China.
FAU - Wang, Peng
AU  - Wang P
AD  - Department of Orthopaedics, Wuxi No. 9 People's Hospital Affiliated to Soochow 
      University, Wuxi 214000 Jiangsu, China.
FAU - Luo, Junhao
AU  - Luo J
AD  - Department of Orthopaedics, Wuxi No. 9 People's Hospital Affiliated to Soochow 
      University, Wuxi 214000 Jiangsu, China.
FAU - Rui, Yongjun
AU  - Rui Y
AUID- ORCID: 0000-0002-1103-2935
AD  - Department of Orthopaedics, Wuxi No. 9 People's Hospital Affiliated to Soochow 
      University, Wuxi 214000 Jiangsu, China.
LA  - eng
PT  - Journal Article
DEP - 20221017
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
RN  - 0 (bcl-2-Associated X Protein)
RN  - EC 2.7.7.31 (DNA Nucleotidylexotransferase)
RN  - TDQ283MPCW (Eosine Yellowish-(YS))
RN  - YKM8PY2Z55 (Hematoxylin)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Male
MH  - Rats
MH  - Apoptosis/genetics/physiology
MH  - bcl-2-Associated X Protein/genetics/metabolism
MH  - DNA Nucleotidylexotransferase
MH  - Eosine Yellowish-(YS)
MH  - Hematoxylin
MH  - *p38 Mitogen-Activated Protein Kinases/genetics/metabolism
MH  - Rats, Sprague-Dawley
MH  - *Reperfusion Injury/genetics/metabolism
MH  - *Surgical Flaps/blood supply/physiology
MH  - *Skin/blood supply/metabolism
MH  - Dermatologic Surgical Procedures
PMC - PMC9592197
COIS- The authors declare that they have no conflicts of interest.
EDAT- 2022/10/28 06:00
MHDA- 2022/10/29 06:00
PMCR- 2022/10/17
CRDT- 2022/10/27 02:28
PHST- 2022/08/26 00:00 [received]
PHST- 2022/09/28 00:00 [revised]
PHST- 2022/09/30 00:00 [accepted]
PHST- 2022/10/27 02:28 [entrez]
PHST- 2022/10/28 06:00 [pubmed]
PHST- 2022/10/29 06:00 [medline]
PHST- 2022/10/17 00:00 [pmc-release]
AID - 10.1155/2022/1175078 [doi]
PST - epublish
SO  - Oxid Med Cell Longev. 2022 Oct 17;2022:1175078. doi: 10.1155/2022/1175078. 
      eCollection 2022.