Previous articles have shown the protective effects of BDNF for nerve cells by directly preventing drug and chemical inflammation and apoptosis of nerve cells and thereby preventing Parkinson's disease and Alzheimer's.
Similarly, this protective effect has now been shown for pancreatic cells. Pretreatment with BDNF prevented cell inflammation and cell death via toxic drugs used to cause diabetes in vivo.
Cells that are metabolically healthy are not just metabolically heathy, non diabetic cells but have resilience and resistance to cancer transformation. It is also obvious that metabolic health is associated with BDNF levels and that malignant cells are adversely affected by increasing BDNF or activation of the starvation gene set.
BDNF is one of 44 genes in the starvation set whose nuclear transcription is promoted by BHB.
BHB is increased by the following:
Fasting.
Exercise.
MCT or coconut oil.
Ppar alpha agonists such as Ursolic acid, Reservatrol, and Betain.
Telmisartan, Atorvastatin, Fenofibrate.
BDNF protects pancreatic β cells (RIN5F) against cytotoxic action of alloxan, streptozotocin, doxorubicin and benzo(a)pyrene in vitro
Abstract
Objective
The study was conducted to observe whether brain-derived neurotrophic factor (BDNF) has cytoprotective actions against alloxan (AL), streptozotocin (STZ), doxorubicin (DB) and benzo(a)pyrene (BP) compounds in vitro that may account for its beneficial action in diabetes mellitus.
Materials and methods
This in vitro study was performed using rat insulinoma (RIN5F) cells. Possible cytoprotective action of BDNF (using pre-treatment, simultaneous and post-treatment schedules of RIN5F cells with BDNF) against the four chemicals tested was evaluated using MTT and apoptosis assays. Possible mechanism of cytoprotective action of BDNF was assessed by measuring BCl2/IKB-β/Pdx mRNA transcripts and anti-oxidant levels in RIN5F cells. Effect of alloxan, STZ, doxorubicin and BP on the production of BDNF by RIN5F cells was also studied.
Results
Results of the present study revealed that BDNF in the doses (100 ng > 50 ng > 10 ng/ml) has significant cytoprotection (P < 0.001, P < 0.01) on cytotoxic action of AL, STZ, DB and BP against rat insulinoma RIN5F (5 × 104 cells/100 μl) cells in vitro. It was observed that AL, STZ, DB and BP inhibited BDNF production significantly (P < 0.001) in a dose-dependent manner by RIN5F cells (0.5 × 106 cells/500 μl) in vitro, while BDNF not only prevented apoptosis induced by these four chemicals but also significantly increased (P < 0.001) BCl2/IKB-β/Pdx mRNA transcripts and restored anti-oxidant levels (P < 0.01) in RIN5F cells to normal.
Discussion
These results suggest that BDNF has potent cytoprotective actions, restores anti-oxidant defenses to normal and thus, prevents apoptosis and preserves insulin secreting capacity of β cells. In addition, BDNF enhanced viability of RIN 5F in vitro. Thus, BDNF not only has anti-diabetic actions but also preserves pancreatic β cells integrity and enhances their viability. These results imply that BDNF functions as an endogenous cytoprotective molecule that may explain its beneficial actions in some neurological conditions as well
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