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TNF-α and IL-10 as paracrine effect of encapsulated mesenchymal stem cells coating by platelet lysate Sibuea, Christine Verawaty; Sitanggang, Ervina Julien; Simaremare, Ade Pryta; Silaen, Rachel Teodora; Kuara , Glenessa; Samosir, Sarah Christina; Ginting, Kharnis Marsha Madora; Yana, Hiqmah Yusi; Pratama, Gita; Mutiara, Mutiara; Angeline, Wiedya Kristianti
Science Midwifery Vol 11 No 6 (2024): February: Midwifery and Health Sciences
Publisher : Institute of Computer Science (IOCS)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.35335/midwifery.v11i6.1427

Abstract

Mesenchymal stem cells (MSCs) have been used as a cellular therapy for infectious and degenerative diseases due to their paracrine effect, immunomodulatory capability, high ability differentiation, and high plasticity. The paracrine effect of MSCs releases many growth factors and pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10), enabling them to modulate the immune system. Nevertheless, there are many obstacles to maintaining paracrine effects in cellular therapy due to a shortage of cellular retention. MSC encapsulation provides a favourable environment for the enhanced viability of MSCs. Platelet lysate is comprised of many growth factors that support the paracrine effect of mesenchymal stem cells (MSCs). In this study, MSCs were encapsulated within alginate, crosslinked using calcium chloride (CaCl2), and subsequently coated with platelet lysate. Encapsulated MSCs coated by platelet lysate were cultured for 21 days and analyzed for IL-10 and TNF-α levels. The findings of our study performed that TNF-α in encapsulated mesenchymal stem cells (MSCs) coated with platelet lysate increased until day 21. IL-10 was retained within the capsule and detected very in day 14. This study showed that encapsulated MSCs coated with platelet lysate affected paracrine effect TNF-α of MSC and retained IL-10 inside the capsule
Hubungan Diabetes Melitus Tipe 2 dengan Penyakit Ginjal Kronis: Tinjauan Literatur: The Relationship Between Type 2 Diabetes Mellitus and Chronic Kidney Disease: A Literature Review Salsabila, Nuzulia Hikmah; Adhayati, Baety; Selfie, Selfie; Harahap, Alfuu Nur; Sitanggang, Ervina Julien; Prameswari, Yuda Nabella
Journal of Health and Physical Vol. 2 No. 1 (2026): April
Publisher : BALE LITERASI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.58218/jhp.v2i1.2703

Abstract

Type 2 diabetes mellitus is a major global health problem and one of the leading causes of chronic kidney disease. Chronic hyperglycemia in diabetes plays a crucial role in the development of kidney damage, which may progress to end-stage renal disease if not properly managed. This review aims to explore the relationship between type 2 diabetes mellitus and chronic kidney disease, focusing on underlying pathophysiological mechanisms and clinical implications. A narrative review approach was conducted using literature from PubMed, ScienceDirect, and Google Scholar published between 2016 and 2026. The findings indicate that persistent hyperglycemia contributes to kidney damage through multiple interconnected mechanisms, including oxidative stress, inflammation, and fibrosis. These processes lead to structural and functional alterations in the kidney, such as glomerular dysfunction, declining glomerular filtration rate, and accumulation of metabolic waste products. Furthermore, the coexistence of diabetes and chronic kidney disease is associated with a higher risk of systemic complications, particularly cardiovascular disease, anemia, and metabolic disturbances, which significantly impact patient outcomes. Overall, type 2 diabetes mellitus and chronic kidney disease have a strong and complex relationship. Effective glycemic control, early detection, and comprehensive monitoring of kidney function are essential strategies to prevent disease progression and reduce the burden of complications, highlighting the importance of integrated management in patients with diabetes.