Involvement of amylin B-H2S-connexin 43 signaling pathway in vascular dysfunction and enhanced ischemia-reperfusion-induced myocardial injury in diabetic rats.

Liu X, Yang R, Bai W, Xu X, Bi F, Hao Y, Yang Q, Li H

Bioscience reports1 Jun 2020Cited by 5 (Europe PMC)

PMID32436936PMCIDPMC7280474DOI10.1042/bsr20194154PepBankPUB-32436936

Summary

The present study was designed to investigate the role of amylin, H2S, and connexin 43 in vascular dysfunction and enhanced ischemia-reperfusion (I/R)-induced myocardial injury in diabetic rats. A single dose of streptozotocin (65 mg/kg) was employed to induce diabetes mellitus. After 8 weeks, there was a significant decrease in the plasma levels of amylin, an increase in I/R injury to isolated hearts (increase in CK-MB and cardiac troponin release) on the Langendorff apparatus. Moreover, there was a significant impairment in vascular endothelium function as assessed by quantifying acetylcholine-induced relaxation in norepinephrine-precontracted mesenteric arteries. There was also a marked decrease in the expression of H2S and connexin 43 in the hearts following I/R injury in diabetic rats. Treatment with amylin agonist, pramlintide (100 and 200 µg/kg), and H2S donor, NaHS (10 and 20 μmol/kg) for 2 weeks improved the vascular endothelium function, abolished enhanced myocardial injury and restored the levels of H2S along with connexin 43 in diabetic animals. However, pramlintide and NaHS failed to produce these effects the presence of gap junction blocker, carbenoxolone (20 and 40 mg/kg). Carbenoxolone also abolished the myocardial levels of connexin 43 without affecting the plasma levels of amylin and myocardial levels of H2S. The decrease in the amylin levels with a consequent reduction in H2S and connexin 43 may contribute to inducing vascular dysfunction and enhancing I/R-induced myocardial injury in diabetic rats.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone5

In this study, Pramlintide (Symlin) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Pramlintide (Symlin).

01AnimalNot a test of Pramlintide (Symlin) aloneAnimal study (in vivo)Efficacy outcome
In diabetic rats, treatment with pramlintide and NaHS improved vascular endothelial function.
In plain wordsIn rats with diabetes, treatment with pramlintide and NaHS improved blood vessel function.
Peptide
Pramlintide (Symlin)
Outcome
IncreaseVascular endothelial function
Study
ratn: not reported in source
Diabetic rats with ischemia-reperfusion injury
Outcome group
Vascular function · Cardiovascular
Source sentences
Summary
Treatment with amylin agonist, pramlintide (100 and 200 µg/kg), and H2S donor, NaHS (10 and 20 μmol/kg) for 2 weeks improved the vascular endothelium function, abolished enhanced myocardial injury and restored the levels of H2S along with connexin 43 in diabetic animals.
1 context sentence(design, population, supporting numbers)
Summary · context
The present study was designed to investigate the role of amylin, H2S, and connexin 43 in vascular dysfunction and enhanced ischemia-reperfusion (I/R)-induced myocardial injury in diabetic rats.
In this study, Pramlintide (Symlin) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Pramlintide (Symlin).
Show in the study text Report a problemFND-3243693601
02AnimalNot a test of Pramlintide (Symlin) aloneAnimal study (in vivo)Efficacy outcome
In diabetic rats, treatment with pramlintide and NaHS abolished enhanced myocardial injury.
In plain wordsIn rats with diabetes, treatment with pramlintide and NaHS removed the increase in heart injury.
Peptide
Pramlintide (Symlin)
Outcome
DecreaseMyocardial injury
Study
ratn: not reported in source
Diabetic rats with ischemia-reperfusion injury
Outcome group
Heart function · Cardiovascular
Source sentences
Summary
Treatment with amylin agonist, pramlintide (100 and 200 µg/kg), and H2S donor, NaHS (10 and 20 μmol/kg) for 2 weeks improved the vascular endothelium function, abolished enhanced myocardial injury and restored the levels of H2S along with connexin 43 in diabetic animals.
1 context sentence(design, population, supporting numbers)
Summary · context
The present study was designed to investigate the role of amylin, H2S, and connexin 43 in vascular dysfunction and enhanced ischemia-reperfusion (I/R)-induced myocardial injury in diabetic rats.
In this study, Pramlintide (Symlin) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Pramlintide (Symlin).
Show in the study text Report a problemFND-3243693602
03AnimalNot a test of Pramlintide (Symlin) aloneAnimal study (in vivo)Mechanism
In diabetic rats, treatment with pramlintide and NaHS restored H2S levels.
In plain wordsIn rats with diabetes, treatment with pramlintide and NaHS restored H2S levels.
Peptide
Pramlintide (Symlin)
Outcome
IncreaseMyocardial H2S levels
Study
ratn: not reported in source
Diabetic rats with ischemia-reperfusion injury
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Treatment with amylin agonist, pramlintide (100 and 200 µg/kg), and H2S donor, NaHS (10 and 20 μmol/kg) for 2 weeks improved the vascular endothelium function, abolished enhanced myocardial injury and restored the levels of H2S along with connexin 43 in diabetic animals.
1 context sentence(design, population, supporting numbers)
Summary · context
The present study was designed to investigate the role of amylin, H2S, and connexin 43 in vascular dysfunction and enhanced ischemia-reperfusion (I/R)-induced myocardial injury in diabetic rats.
In this study, Pramlintide (Symlin) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Pramlintide (Symlin).
Show in the study text Report a problemFND-3243693603
04AnimalNot a test of Pramlintide (Symlin) aloneAnimal study (in vivo)Mechanism
In diabetic rats, treatment with pramlintide and NaHS restored connexin 43 levels.
In plain wordsIn rats with diabetes, treatment with pramlintide and NaHS restored connexin 43 levels.
Peptide
Pramlintide (Symlin)
Outcome
IncreaseMyocardial connexin 43 levels
Study
ratn: not reported in source
Diabetic rats with ischemia-reperfusion injury
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Treatment with amylin agonist, pramlintide (100 and 200 µg/kg), and H2S donor, NaHS (10 and 20 μmol/kg) for 2 weeks improved the vascular endothelium function, abolished enhanced myocardial injury and restored the levels of H2S along with connexin 43 in diabetic animals.
1 context sentence(design, population, supporting numbers)
Summary · context
The present study was designed to investigate the role of amylin, H2S, and connexin 43 in vascular dysfunction and enhanced ischemia-reperfusion (I/R)-induced myocardial injury in diabetic rats.
In this study, Pramlintide (Symlin) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Pramlintide (Symlin).
Show in the study text Report a problemFND-3243693604
05AnimalNot a test of Pramlintide (Symlin) aloneAnimal study (in vivo)Mechanism
In diabetic rats, pramlintide and NaHS failed to produce the reported protective effects in the presence of carbenoxolone.
In plain wordsIn rats with diabetes, pramlintide and NaHS did not produce the reported protective effects when carbenoxolone was present.
Peptide
Pramlintide (Symlin)
Outcome
Not applicableGap junction blockade of treatment effects
Study
ratn: not reported in source
Diabetic rats with ischemia-reperfusion injury
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
However, pramlintide and NaHS failed to produce these effects the presence of gap junction blocker, carbenoxolone (20 and 40 mg/kg).
2 context sentences(design, population, supporting numbers)
Summary · context
Treatment with amylin agonist, pramlintide (100 and 200 µg/kg), and H2S donor, NaHS (10 and 20 μmol/kg) for 2 weeks improved the vascular endothelium function, abolished enhanced myocardial injury and restored the levels of H2S along with connexin 43 in diabetic animals.
Summary · context
The present study was designed to investigate the role of amylin, H2S, and connexin 43 in vascular dysfunction and enhanced ischemia-reperfusion (I/R)-induced myocardial injury in diabetic rats.
In this study, Pramlintide (Symlin) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Pramlintide (Symlin).
Show in the study text Report a problemFND-3243693605

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
22 Oct 2026, 02:26 UTC
Study results updated
Version 1
21 Oct 2026, 18:59 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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