Scientific Reports· 2026Q1
Mezenkimal kök hücreler, diyabetik sıçanlarda PI3K/AKT/mTOR ve TGF-β sinyal yolları aracılığıyla pankreas ve dalak iltihabını modüle eder
Mesenchymal stem cells modulate pancreatic and splenic inflammation through PI3K/AKT/mTOR and TGF-β signalling in diabetic rats
- 0atıf
- Q1SCImago
- 2026yıl
Kısa özet
Mezenkimal kök hücrelerin (MSC) tek bir dozu, diyabetik sıçanlarda apoptoz öncülü genleri (Caspase3, P53) ve stres yanıt genlerini (P38) aşağı regüle ederek ve apoptoz karşıtı genleri (BCL2) yukarı regüle ederek pankreas ve dalak dokusu mimarisini kısmen geri kazandırmıştır.
Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.
Ana noktalar
- MSC tedavisi, diyabetik sıçan pankreas ve dalaklarında Caspase3, P53 ve P38 gen ekspresyonunu aşağı regüle etmiştir.
- MSC tedavisi, apoptoz karşıtı bir belirteç olan BCL2 gen ekspresyonunu yukarı regüle etmiştir.
- Pankreatik ve dalak PI3K ve AKT protein seviyeleri MSC tedavisi ile geri kazanılmıştır.
- Yüksek TGF-β protein ekspresyonu MSC'ler tarafından azaltılmış, ancak mTOR yüksek kalmıştır.
- MSC tedavisi, pankreatik adacık ve dalak dokusu mimarisinin kısmi olarak yeniden yapılandırılmasına yol açmıştır.
Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.
Özet (abstract)
Bone marrow-derived mesenchymal stem cells (MSC) can attenuate diabetic organ damage through immunomodulatory and paracrine mechanisms, yet the specific signalling pathways engaged in the pancreas and spleen remain poorly characterized. This study investigated the effects of a single dose of undifferentiated MSC on PI3K/AKT/mTOR and TGF-β signalling, apoptotic gene expression, and tissue architecture in the pancreas and spleen of streptozotocin (STZ)-induced diabetic rats. Female rats were divided into four groups: control, diabetic (induced by streptozotocin), insulin-treated diabetic, and MSC-treated diabetic. Gene expression levels of SRY, C-Jun, P53, BCL2, P38, and Caspase3 were assessed using quantitative PCR and normalized against GAPDH. Tissue histopathology of the spleen and pancreas using H&E and immunohistochemistry (IHC) staining for PI3K, AKT, mTOR, and TGF-β were investigated. MSC-treated group showed a significant downregulation of pro-apoptotic markers Caspase3 and P53, and stress response genes P38 with upregulated anti-apoptotic gene BCL2 compared to the untreated diabetic rats. Pancreatic and splenic PI3K and AKT protein were restored following MSC treatment. Conversely, elevated TGF-β protein expression was reduced by MSC therapy, whereas mTOR remained elevated in MSC-treated tissues while lowered toward control levels by insulin. These molecular changes were accompanied by partial restoration of islet architecture and splenic histology. To our knowledge, this is among few studies concurrently characterized PI3K/AKT/mTOR and TGF-β signaling in both pancreatic and splenic tissues from the same diabetic animal. MSC therapy demonstrates a potential therapeutic role by modulating inflammatory and cell apoptotic pathways of PI3K/AKT/mTOR and TGF-β signalling with partial preservation of pancreatic and splenic tissue. A differential mTOR response was observed, whereby insulin, but not MSC treatment, restored mTOR expression toward control levels. Our findings support MSC further investigation as a regenerative adjunct to conventional diabetes management.
Yazarların özeti; kaynağından alınmıştır. Scientific Reports, 2026 · DOI ↗
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Alan: Genetik (Tıp)
GeneticsMedicine