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Combined Systemic Intake of K-ATP Opener (Nicorandil) and Mesenchymal Stem Cells Preconditioned With Nicorandil Alleviates Pancreatic Insufficiency in a Model of Bilateral Renal Ischemia/Reperfusion Injury

ShamsEldeen, Asmaa Mohammed ; El-Aal, Sarah A. Abd ; Aboulhoda, Basma Emad ; AbdAllah, Hend ; Gamal, Sara Mahmoud ; Hassan, Fatma E. ; Mehesen, Marwa Nagi ; Rashed, Laila Ahmed ; Mostafa, Abeer ; Sadek, Nermeen Bakr

Frontiers in physiology, 2022-06, Vol.13, p.934597-934597 [Peer Reviewed Journal]

Frontiers Media S.A

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  • Title:
    Combined Systemic Intake of K-ATP Opener (Nicorandil) and Mesenchymal Stem Cells Preconditioned With Nicorandil Alleviates Pancreatic Insufficiency in a Model of Bilateral Renal Ischemia/Reperfusion Injury
  • Author: ShamsEldeen, Asmaa Mohammed ; El-Aal, Sarah A. Abd ; Aboulhoda, Basma Emad ; AbdAllah, Hend ; Gamal, Sara Mahmoud ; Hassan, Fatma E. ; Mehesen, Marwa Nagi ; Rashed, Laila Ahmed ; Mostafa, Abeer ; Sadek, Nermeen Bakr
  • Subjects: bilateral renal I/R ; MSc ; nicorandil ; pancreatic damage ; Physiology ; PI3K/AKT/mTOR
  • Is Part Of: Frontiers in physiology, 2022-06, Vol.13, p.934597-934597
  • Notes: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
    Reviewed by: Jorge Sanchez, Instituto Politécnico Nacional de México (CINVESTAV), Mexico
    This article was submitted to Integrative Physiology, a section of the journal Frontiers in Physiology
    Edited by: Andrei Krivtsov, Dana–Farber Cancer Institute, United States
    Qi Wan, Qingdao University, China
  • Description: We used nicorandil, a K-ATP channel opener, to study the role of these channels in the amelioration of renal ischemia/reperfusion (I/R)-induced pancreatic injury, and the possible involvement of PI3K/Akt/mTOR signaling pathway. Forty-two male Wistar rats were included in this study, six were sacrificed for extraction of bone marrow mesenchymal stem cells (BM-MSCs) and conducting the in-vitro work, the others were included in vivo study and equally divided into six groups. Group 1 (sham control), but groups 2–6 were subjected to bilateral renal I/R: Group 2 (I/R); Group 3 (I/R-NC), treated with nicorandil; Group 4 (I/R-MSCs), treated with BM-MSCs; Group 5 (I/R-MSCC), treated with nicorandil-preconditioned BM-MSCs; Group 6 (I/R-NC-MSCC), treated with both systemic nicorandil and preconditioned BM-MSCC. Renal injury and subsequent pancreatic damage were detected in the I/R group by a significant increase in serum urea, creatinine, fasting glucose, and pancreatic enzymes. The pancreatic tissues showed a reduction in cellularity and a significant decrease in the expression of the cell survival pathway, PI3K/Akt/mTOR, in the I/R group compared to the control. Preconditioning MSCs with nicorandil significantly enhanced the proliferation assay and decreased their apoptotic markers. Indeed, combined systemic nicorandil and nicorandil-preconditioning maintained survival of MSC in the pancreatic tissue and amelioration of apoptotic markers and pancreatic TNF-α production. Histologically, all treated groups revealed better pancreatic architecture, and increased area % of anti-insulin antibody and CD31, which were all best observed in the NC-MSCC group. Thus, using K-ATP channel opener was efficient to enhance PI3K/Akt/mTOR expression levels ( in vivo and in vitro ).
  • Publisher: Frontiers Media S.A
  • Language: English
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