Calcitonin Gene-Related Peptide Downregulates Expression of Inducible Nitride Oxide Synthase and Caspase-3 after Intestinal Ischemia-Reperfusion Injury in Rats

Chih Cheng Luo, Jhen-Sheng Huang, Yung Ching Ming, Shih Ming Chu, Hsun Chin Chao

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background: Various investigations have demonstrated that calcitonin gene-related peptide (CGRP) plays an important role in mediating ischemic preconditioning. CGRP has been shown to mimic the protective effects of ischemic preconditioning and mitigate ischemia-reperfusion (I/R) injury in the heart, brain, gastrointestinal system, and other tissues. This study aimed to examine whether CGRP, a proven intestinal cytoprotective molecule, exerted its protective effects through modulation of inducible nitride oxide synthase (iNOS) and apoptosis after intestinal I/R injury. Methods: This animal study randomly divided 30 rats into the following five groups: (1) the normal control group, (2) the ischemia group with normal saline, (3) the I/R group with normal saline, (4) the ischemia group with CGRP (300 μg/kg), and (5) the I/R group with CGRP (300 μg/kg). Levels of iNOS messenger RNA (mRNA) and protein, and caspase-3 protein were determined by real-time quantitative polymerase chain reaction and Western blotting analyses, respectively. Statistical analysis was performed using analysis of variance with Dunn test. Results: The mRNA levels of iNOS increased after the intestinal ischemia or intestinal reperfusion phase (p <0.01), and CGRP pretreatment significantly decreased iNOS mRNAs and protein levels (p <0.01). The expression protein levels of caspase-3 increased after the intestinal ischemia or intestinal reperfusion phase. CGRP pretreatment significantly decreased the levels of caspase-3 proteins. CGRP intestinal cytoprotection is mediated, in part, by downregulation of expression of iNOS and caspase-3 after intestinal I/R injury. Conclusion: The study indicates that the cytoprotective role of CGRP (i.e., antiapoptotic effect) after I/R injury could be via downregulation of iNOS, which may relieve I/R tissue damage by blocking iNOS activity.

Original languageEnglish
Pages (from-to)474-479
JournalPediatrics and Neonatology
Volume57
Issue number6
DOIs
Publication statusPublished - Dec 1 2016

Fingerprint

Calcitonin Gene-Related Peptide
Reperfusion Injury
Caspase 3
Oxides
Down-Regulation
Ischemia
Reperfusion
Ischemic Preconditioning
Proteins
Messenger RNA
Cytoprotection
Real-Time Polymerase Chain Reaction
Analysis of Variance
Western Blotting
Apoptosis
Control Groups
Brain

Keywords

  • calcitonin gene-related peptide
  • Caspase-3
  • Inducible nitride oxide synthase
  • Ischemia-reperfusion injury
  • Small intestine

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Calcitonin Gene-Related Peptide Downregulates Expression of Inducible Nitride Oxide Synthase and Caspase-3 after Intestinal Ischemia-Reperfusion Injury in Rats. / Luo, Chih Cheng; Huang, Jhen-Sheng; Ming, Yung Ching; Chu, Shih Ming; Chao, Hsun Chin.

In: Pediatrics and Neonatology, Vol. 57, No. 6, 01.12.2016, p. 474-479.

Research output: Contribution to journalArticle

Luo, Chih Cheng ; Huang, Jhen-Sheng ; Ming, Yung Ching ; Chu, Shih Ming ; Chao, Hsun Chin. / Calcitonin Gene-Related Peptide Downregulates Expression of Inducible Nitride Oxide Synthase and Caspase-3 after Intestinal Ischemia-Reperfusion Injury in Rats. In: Pediatrics and Neonatology. 2016 ; Vol. 57, No. 6. pp. 474-479.
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abstract = "Background: Various investigations have demonstrated that calcitonin gene-related peptide (CGRP) plays an important role in mediating ischemic preconditioning. CGRP has been shown to mimic the protective effects of ischemic preconditioning and mitigate ischemia-reperfusion (I/R) injury in the heart, brain, gastrointestinal system, and other tissues. This study aimed to examine whether CGRP, a proven intestinal cytoprotective molecule, exerted its protective effects through modulation of inducible nitride oxide synthase (iNOS) and apoptosis after intestinal I/R injury. Methods: This animal study randomly divided 30 rats into the following five groups: (1) the normal control group, (2) the ischemia group with normal saline, (3) the I/R group with normal saline, (4) the ischemia group with CGRP (300 μg/kg), and (5) the I/R group with CGRP (300 μg/kg). Levels of iNOS messenger RNA (mRNA) and protein, and caspase-3 protein were determined by real-time quantitative polymerase chain reaction and Western blotting analyses, respectively. Statistical analysis was performed using analysis of variance with Dunn test. Results: The mRNA levels of iNOS increased after the intestinal ischemia or intestinal reperfusion phase (p <0.01), and CGRP pretreatment significantly decreased iNOS mRNAs and protein levels (p <0.01). The expression protein levels of caspase-3 increased after the intestinal ischemia or intestinal reperfusion phase. CGRP pretreatment significantly decreased the levels of caspase-3 proteins. CGRP intestinal cytoprotection is mediated, in part, by downregulation of expression of iNOS and caspase-3 after intestinal I/R injury. Conclusion: The study indicates that the cytoprotective role of CGRP (i.e., antiapoptotic effect) after I/R injury could be via downregulation of iNOS, which may relieve I/R tissue damage by blocking iNOS activity.",
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T1 - Calcitonin Gene-Related Peptide Downregulates Expression of Inducible Nitride Oxide Synthase and Caspase-3 after Intestinal Ischemia-Reperfusion Injury in Rats

AU - Luo, Chih Cheng

AU - Huang, Jhen-Sheng

AU - Ming, Yung Ching

AU - Chu, Shih Ming

AU - Chao, Hsun Chin

PY - 2016/12/1

Y1 - 2016/12/1

N2 - Background: Various investigations have demonstrated that calcitonin gene-related peptide (CGRP) plays an important role in mediating ischemic preconditioning. CGRP has been shown to mimic the protective effects of ischemic preconditioning and mitigate ischemia-reperfusion (I/R) injury in the heart, brain, gastrointestinal system, and other tissues. This study aimed to examine whether CGRP, a proven intestinal cytoprotective molecule, exerted its protective effects through modulation of inducible nitride oxide synthase (iNOS) and apoptosis after intestinal I/R injury. Methods: This animal study randomly divided 30 rats into the following five groups: (1) the normal control group, (2) the ischemia group with normal saline, (3) the I/R group with normal saline, (4) the ischemia group with CGRP (300 μg/kg), and (5) the I/R group with CGRP (300 μg/kg). Levels of iNOS messenger RNA (mRNA) and protein, and caspase-3 protein were determined by real-time quantitative polymerase chain reaction and Western blotting analyses, respectively. Statistical analysis was performed using analysis of variance with Dunn test. Results: The mRNA levels of iNOS increased after the intestinal ischemia or intestinal reperfusion phase (p <0.01), and CGRP pretreatment significantly decreased iNOS mRNAs and protein levels (p <0.01). The expression protein levels of caspase-3 increased after the intestinal ischemia or intestinal reperfusion phase. CGRP pretreatment significantly decreased the levels of caspase-3 proteins. CGRP intestinal cytoprotection is mediated, in part, by downregulation of expression of iNOS and caspase-3 after intestinal I/R injury. Conclusion: The study indicates that the cytoprotective role of CGRP (i.e., antiapoptotic effect) after I/R injury could be via downregulation of iNOS, which may relieve I/R tissue damage by blocking iNOS activity.

AB - Background: Various investigations have demonstrated that calcitonin gene-related peptide (CGRP) plays an important role in mediating ischemic preconditioning. CGRP has been shown to mimic the protective effects of ischemic preconditioning and mitigate ischemia-reperfusion (I/R) injury in the heart, brain, gastrointestinal system, and other tissues. This study aimed to examine whether CGRP, a proven intestinal cytoprotective molecule, exerted its protective effects through modulation of inducible nitride oxide synthase (iNOS) and apoptosis after intestinal I/R injury. Methods: This animal study randomly divided 30 rats into the following five groups: (1) the normal control group, (2) the ischemia group with normal saline, (3) the I/R group with normal saline, (4) the ischemia group with CGRP (300 μg/kg), and (5) the I/R group with CGRP (300 μg/kg). Levels of iNOS messenger RNA (mRNA) and protein, and caspase-3 protein were determined by real-time quantitative polymerase chain reaction and Western blotting analyses, respectively. Statistical analysis was performed using analysis of variance with Dunn test. Results: The mRNA levels of iNOS increased after the intestinal ischemia or intestinal reperfusion phase (p <0.01), and CGRP pretreatment significantly decreased iNOS mRNAs and protein levels (p <0.01). The expression protein levels of caspase-3 increased after the intestinal ischemia or intestinal reperfusion phase. CGRP pretreatment significantly decreased the levels of caspase-3 proteins. CGRP intestinal cytoprotection is mediated, in part, by downregulation of expression of iNOS and caspase-3 after intestinal I/R injury. Conclusion: The study indicates that the cytoprotective role of CGRP (i.e., antiapoptotic effect) after I/R injury could be via downregulation of iNOS, which may relieve I/R tissue damage by blocking iNOS activity.

KW - calcitonin gene-related peptide

KW - Caspase-3

KW - Inducible nitride oxide synthase

KW - Ischemia-reperfusion injury

KW - Small intestine

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