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Anti-inflammatory and antioxidant potential capacities of AD-MSCs and BM-MSCs in suppressing pancreatic β-cells auto-immunity and apoptosis in rats with T1DM induced model

SHADY G. EL-SAWAH1,*, FAYEZ ALTHOBAITI2, HANAN M. RASHWAN1, ADIL ALDHAHRANI3, MARWA A. ABDEL-DAYEM4, EMAN FAYAD2, REHAB M. AMEN5, EL SHAIMAA SHABANA6, EHAB I. EL-HALLOUS7

1 Zoology Department, Faculty of Science, Arish University, North Sinai, Egypt
2 Biotechnology Department, Faculty of Science, Taif University, Taif, Saudi Arabia
3 Clinical Laboratory Science Department, Turabah University College, Taif University, Taif, Saudi Arabia
4 Department of Pharmacology and Biochemistry, Faculty of Pharmacy, Horus University-Egypt, New Damietta, Egypt
5 Biology Department, College of Science, University of Bisha, Bisha, Saudi Arabia
6 Fellow of Biochemistry, Genetic Unit, Children Hospital, Faculty of Medicine, Mansoura University, Dakahlia Governorate, Egypt
7 Biology Department, Faculty of Science, Taif University, Taif, Saudi Arabia

* Corresponding Author: SHADY G. EL-SAWAH. Email: email

(This article belongs to the Special Issue: Cell-Based Regenerative Therapies)

BIOCELL 2022, 46(3), 745-757. https://doi.org/10.32604/biocell.2022.017853

Abstract

Since Type 1 diabetes (T1DM) occurs when β-cells mass is reduced to less than 20% of the normal level due to autoimmune destruction of cells resulting in the inability to secrete insulin, preservation or replenishment of the functional β-cells mass has become a major therapeutic focus for this diabetic type treatment. Thus, this 4-week work plan was designed to determine which mesenchymal stem cells (MSCs) type is more appropriate to alleviate pancreatic hazards resulting from diabetes induction; via tracking a comparative study between MSCs derived from adipose tissue (AD-MSCs) and from bone marrow (BM-MSCs) in management of T1DM considering their immunomodulatory, anti-apoptotic and antioxidative roles. Rats were divided randomly into 4 groups; control, STZ-diabetic (D), D+AD-MSCs, and D+BM-MSCs groups. Both stem cells types in this study were allogenic. Herein, both oxidative stress and antioxidant markers were evaluated using colorimetric analysis, while inflammatory, immune and apoptotic markers were assessed through flow cytometric analysis. Results showed that diabetic rats treated with either AD-MSCs or BM-MSCs exhibited marked pancreatic antioxidant and anti-inflammatory activities that were able to initiate pancreatic immunomodulation and reducing β-cells apoptotic death, thus, help to restore their normal insulin secretion and hypoglycemic abilities. However, AD-MSCs injection was shown to be superior as a pancreatic regenerative tool in overcoming diabetes; owing to their marked antioxidant, anti-inflammatory, immunomodulatory, and anti-apoptotic characteristics over BM-MSCs treatment.

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APA Style
EL-SAWAH, S.G., ALTHOBAITI, F., RASHWAN, H.M., ALDHAHRANI, A., ABDEL-DAYEM, M.A. et al. (2022). Anti-inflammatory and antioxidant potential capacities of ad-mscs and bm-mscs in suppressing pancreatic β-cells auto-immunity and apoptosis in rats with T1DM induced model. BIOCELL, 46(3), 745-757. https://doi.org/10.32604/biocell.2022.017853
Vancouver Style
EL-SAWAH SG, ALTHOBAITI F, RASHWAN HM, ALDHAHRANI A, ABDEL-DAYEM MA, FAYAD E, et al. Anti-inflammatory and antioxidant potential capacities of ad-mscs and bm-mscs in suppressing pancreatic β-cells auto-immunity and apoptosis in rats with T1DM induced model. BIOCELL . 2022;46(3):745-757 https://doi.org/10.32604/biocell.2022.017853
IEEE Style
S.G. EL-SAWAH et al., “Anti-inflammatory and antioxidant potential capacities of AD-MSCs and BM-MSCs in suppressing pancreatic β-cells auto-immunity and apoptosis in rats with T1DM induced model,” BIOCELL , vol. 46, no. 3, pp. 745-757, 2022. https://doi.org/10.32604/biocell.2022.017853



cc Copyright © 2022 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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