In vitro differentiation of human pancreatic duct–derived PANC-1 cells into β-cell phenotype using Tinospora cordifolia

Communal interaction of glycation and gut microbes in diabetes mellitus, Alzheimer's disease, and Parkinson's disease pathogenesis

“…These strategies include bioactive molecules like eugenol, 142 geraniol, 377 limonene, 378,379 and so forth, solely and in combination with aminoguanidine. We also showed that by using Tinospora cordifolia , it is possible to differentiate human pancreatic duct–derived PANC‐1 cells into functional beta cells 380 . After providing in vitro cytokine cocktail‐based model to assess and screen compounds that can protect apoptosis of β‐cells and retard the progress of T1DM, 381 in another interesting study, we proved that aqueous extract of Curcuma longa and Piper nigrum were able to protect β‐cells against apoptosis and can be implemented as an oral herbal treatment for T1DM 382 .…”

“…We also showed that by using Tinospora cordifolia, it is possible to differentiate human pancreatic duct-derived PANC-1 cells into functional beta cells. 380 After providing in vitro cytokine cocktail-based model to assess and screen compounds that can protect apoptosis of β-cells and retard the progress of T1DM, 381 in another interesting study, we proved that aqueous extract of Curcuma longa and Piper nigrum were able to protect β-cells against apoptosis and can be implemented as an oral herbal treatment for T1DM. 382 Considering other studies, researchers addressed the natural compound "C-Phycocyanin" as an effective pigment protein in T2DM.…”

Regeneration of Pancreatic Beta Cells by Modulation of Molecular Targets Using Plant-Derived Compounds: Pharmacological Mechanisms and Clinical Potential

“…Various plant extracts and compounds have displayed a capacity to activate neogenetic processes in different experimental models of diabetes. Not indicated [83] Note: ↑ depicts an increase in mRNA or protein expression or activity, ↓ depicts a decrease in mRNA or protein expression or activity…”

“…The delineation between neogenesis and transdifferentiation can be confusing because studies have identified progenitor cells within the pancreatic ductal structures, while duct cells have also been shown to differentiate into insulin-producing beta-like cells following reprograming using a cocktail of Pdx-1, Ngn3 and MafA transcription factors (Spears et al, 2021). However, in the studies summarized in the current review, geniposide [ 64 ], T. cordifolia [ 83 ], O. integrifolia [ 78 ], puerarin [ 79 ], swertisin [ 47 ], conophylline [ 58 ] and andrographolide [ 56 ] mediated their beta-cell regenerative effects via the transdifferentiation of acinar or ductal cells into beta/beta-like cells. Transdifferentiation of these cells into beta cells was associated with a decreased expression of carbonic anhydrase 9 and an increased expression of pro-endocrine Ngn3, nestin, neuroD1, Nkx2.2, Pdx-1 and MafA [ 47 , 56 , 58 , 64 , 78 , 79 , 83 ].…”

“…However, in the studies summarized in the current review, geniposide [ 64 ], T. cordifolia [ 83 ], O. integrifolia [ 78 ], puerarin [ 79 ], swertisin [ 47 ], conophylline [ 58 ] and andrographolide [ 56 ] mediated their beta-cell regenerative effects via the transdifferentiation of acinar or ductal cells into beta/beta-like cells. Transdifferentiation of these cells into beta cells was associated with a decreased expression of carbonic anhydrase 9 and an increased expression of pro-endocrine Ngn3, nestin, neuroD1, Nkx2.2, Pdx-1 and MafA [ 47 , 56 , 58 , 64 , 78 , 79 , 83 ]. This expression of pro-endocrine markers and the loss of ductal cell differentiation marker carbonic anhydrase 9 [ 83 ] supports the initial de-differentiation of these cells into a progenitor-like status and thereafter, the differentiation of these progenitor-like cells into beta-like endocrine cells.…”