Authors: Kaviani, Maryam
Keshtkar, Somayeh
Azarpira, Negar
Hossein Aghdaei, Mahdokht
Geramizadeh, Bita
Karimi, Mohammad Hossein
Yaghobi, Ramin
Esfandiari, Elaheh
Shamsaeefar, Alireza
Nikeghbalian, Saman
Al-Abdullah, Ismail H.
Title: Cytoprotective effects of ginsenoside Rd on apoptosis-associated cell death in the isolated human pancreatic islets
Language (ISO): en
Abstract: Ginsenoside Rd (GS-Rd), one of the main pharmacologically active components of ginseng, has shown the poten- tial to stabilize mitochondrial membrane integrity and decr ease apoptotic death in neuronal and non-neuronal cells. The present study aimed to evaluate the effect of this bi oactive molecule on the apopto sis-associated cell death in human pancreatic islets. In this regard human pancreatic islets were isolated and grouped for the treatment with GS-Rd. The isolated islets were treated with different concentrations of GS-Rd. After 24 and 72 h of incubation, the islets were evaluated in terms of viability, BAX , BCL2 , and insulin gene expression, BAX, BCL2, and caspase- 3 protein expression, apoptosis, and glucose-induced insu lin/C-peptide secretion. Our results revealed the islet survival was significantly decreased in the control group after 72 h of incubation. However, GS-Rd inhibited the progress of the islet death in the treated groups. TUNEL st aining revealed that the prev entive effect of this mole- cule was caused by the inhibition of apoptosis-associated death. In this regard, th e activation of caspase-3 was down-regulated in the presence of GS-Rd. GS-Rd did not exhibit undesirable effects on glucose-induced insulin and C-peptide stimulation secretion. In conclusion, GS-Rd inhibited the progress of death of cultured human pan- creatic islets by diminishing the apoptosis of the islet cells.
Subject Headings: Apoptosis
Culture
Ginsenoside Rd
Human pancreatic islets
Insulin
Transplantation
URI: http://hdl.handle.net/2003/39045
http://dx.doi.org/10.17877/DE290R-20964
Issue Date: 2019-08-22
Rights link: http://creativecommons.org/licenses/by/4.0/
Appears in Collections:Original Articles

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