PMID- 33433807
OWN - NLM
STAT- MEDLINE
DCOM- 20211209
LR  - 20240226
IS  - 1573-2568 (Electronic)
IS  - 0163-2116 (Print)
IS  - 0163-2116 (Linking)
VI  - 66
IP  - 12
DP  - 2021 Dec
TI  - Mesenteric Lymph Duct Ligation Alleviates Acute Lung Injury Caused by Severe 
      Acute Pancreatitis Through Inhibition of High Mobility Group Box 1-Induced 
      Inflammation in Rats.
PG  - 4344-4353
LID - 10.1007/s10620-020-06801-6 [doi]
AB  - BACKGROUND: Acute lung injury (ALI) is the most common complication and one of 
      the leading causes of mortality of severe acute pancreatitis (SAP). Nevertheless, 
      no effective therapeutic schemes are presently available. AIMS: To investigate 
      the effect and potential mechanism of mesenteric lymph duct ligation (MLDL) on 
      experimental SAP-induced ALI. METHODS: Immediately following MLDL, rats were 
      subjected to SAP by retrograde injection of 5% sodium taurocholate into the 
      biliopancreatic duct. At 24 h after modeling, tissues were collected for 
      morphological examination. The levels of TNF-alpha, IL-6, intercellular adhesion 
      molecule-1 (ICAM1), diamine oxidase (DAO), and D-lactic acid (D-LA) in serum, and 
      the myeloperoxidase (MPO) activity in lung tissues were determined. Moreover, the 
      expressions of high mobility group box 1 (HMGB1), receptor of advanced glycation 
      endproducts (RAGE), and NF-kappaB p65 at the mRNA and protein levels in lung tissues, 
      and the expressions of HMGB1, RAGE, and TNF-alpha at the mRNA level in intestinal 
      lymphoid tissues were evaluated. RESULTS: MLDL significantly attenuated the 
      histological injury of the pancreas and lung and reduced the production of TNF-alpha, 
      IL-6, and ICAM1. Besides, MLDL repressed the activity of MPO in the lung. 
      However, the levels of serum DAO and D-LA were decreased without obvious 
      morphological improvement in intestinal injury. Moreover, MLDL apparently reduced 
      the up-regulation of HMGB1, RAGE, and NF-kappaB p65 in lung tissues, as well as the 
      expressions of HMGB1, RAGE, and TNF-alpha in intestinal lymphoid tissues. 
      CONCLUSIONS: Mesenteric lymph was a source of harmful factors leading to SAP-ALI. 
      MLDL could alleviate SAP-ALI probably by inhibiting HMGB1-induced production of 
      inflammation factors.
CI  - (c) 2021. The Author(s).
FAU - Tang, Yishuang
AU  - Tang Y
AD  - Department of Gastroenterology, Yueyang Hospital of Integrated Traditional 
      Chinese and Western Medicine, Shanghai University of Traditional Chinese 
      Medicine, Shanghai, China.
FAU - Kong, Jing
AU  - Kong J
AD  - Department of Gastroenterology, Yueyang Hospital of Integrated Traditional 
      Chinese and Western Medicine, Shanghai University of Traditional Chinese 
      Medicine, Shanghai, China.
FAU - Zhou, Bingduo
AU  - Zhou B
AUID- ORCID: 0000-0001-7036-4721
AD  - Department of Gastroenterology, Yueyang Hospital of Integrated Traditional 
      Chinese and Western Medicine, Shanghai University of Traditional Chinese 
      Medicine, Shanghai, China. bingduozhou@163.com.
FAU - Wang, Xiaosu
AU  - Wang X
AD  - Department of Gastroenterology, Yueyang Hospital of Integrated Traditional 
      Chinese and Western Medicine, Shanghai University of Traditional Chinese 
      Medicine, Shanghai, China.
FAU - Liu, Xiaowen
AU  - Liu X
AD  - Department of Gastroenterology, Yueyang Hospital of Integrated Traditional 
      Chinese and Western Medicine, Shanghai University of Traditional Chinese 
      Medicine, Shanghai, China.
FAU - Wang, Yi
AU  - Wang Y
AD  - Department of Gastroenterology, Yueyang Hospital of Integrated Traditional 
      Chinese and Western Medicine, Shanghai University of Traditional Chinese 
      Medicine, Shanghai, China.
FAU - Zhu, Shengliang
AU  - Zhu S
AD  - Department of Gastroenterology, Yueyang Hospital of Integrated Traditional 
      Chinese and Western Medicine, Shanghai University of Traditional Chinese 
      Medicine, Shanghai, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20210112
PL  - United States
TA  - Dig Dis Sci
JT  - Digestive diseases and sciences
JID - 7902782
RN  - 0 (Ager protein, rat)
RN  - 0 (HMGB1 Protein)
RN  - 0 (Hbp1 protein, rat)
RN  - 0 (Receptor for Advanced Glycation End Products)
RN  - 0 (Transcription Factor RelA)
RN  - 5E090O0G3Z (Taurocholic Acid)
SB  - IM
MH  - Acute Lung Injury/etiology/*prevention & control
MH  - Animals
MH  - HMGB1 Protein/*metabolism
MH  - Intestinal Mucosa/injuries
MH  - Ligation
MH  - Lung/metabolism
MH  - Lymphatic Vessels/*surgery
MH  - Lymphoid Tissue/metabolism
MH  - Male
MH  - Pancreatitis/*complications/metabolism
MH  - Random Allocation
MH  - Rats, Sprague-Dawley
MH  - Receptor for Advanced Glycation End Products/metabolism
MH  - Taurocholic Acid
MH  - Transcription Factor RelA/metabolism
MH  - Rats
PMC - PMC8589802
OTO - NOTNLM
OT  - Acute lung injury
OT  - HMGB1
OT  - Mesenteric lymph
OT  - Severe acute pancreatitis
COIS- The authors declare no conflicts of interest.
EDAT- 2021/01/13 06:00
MHDA- 2021/12/15 06:00
PMCR- 2021/01/12
CRDT- 2021/01/12 12:23
PHST- 2020/08/12 00:00 [received]
PHST- 2020/12/16 00:00 [accepted]
PHST- 2021/01/13 06:00 [pubmed]
PHST- 2021/12/15 06:00 [medline]
PHST- 2021/01/12 12:23 [entrez]
PHST- 2021/01/12 00:00 [pmc-release]
AID - 10.1007/s10620-020-06801-6 [pii]
AID - 6801 [pii]
AID - 10.1007/s10620-020-06801-6 [doi]
PST - ppublish
SO  - Dig Dis Sci. 2021 Dec;66(12):4344-4353. doi: 10.1007/s10620-020-06801-6. Epub 
      2021 Jan 12.