Oxidative brain and cerebellum injury in diabetes and prostate cancer model: Protective effect of metformin.
Eda DagsuyuPinar Koroglu AydinIlknur Bugan GulOmur Karabulut BulanRefiye YanardagPublished in: Journal of biochemical and molecular toxicology (2023)
The body can host the spread of prostate cancer cells. Metastases from prostate cancer are more frequently seen in the brain, liver, lungs, and lymph nodes. A well-known antidiabetic drug, metformin, is also known to have antitumor effects. Our study focuses on the evaluation of potential metformin protective effects on brain and cerebellum damage in streptozotocin (STZ)-induced diabetic and Dunning prostate cancer models. In this investigation, six groups of male Copenhagen rats were created: control, diabetic (D), cancer (C), diabetic + cancer (DC), cancer + metformin, and diabetic + cancer + metformin. The brain and cerebellum tissues of the rats were taken after sacrifice. Oxidative stress markers including reduced glutathione level, lipid peroxidation, glutathione reductase, glutathione peroxidase, glutathione-S-transferase, catalase, superoxide dismutase activities, reactive oxygen species, total oxidant and total antioxidant status, lactate dehydrogenase, xanthine oxidase, acetylcholinesterase activities, protein carbonyl contents, nitric oxide and OH-proline levels, sodium potassium ATPase, carbonic anhydrase, and glucose-6-phosphate dehydrogenase activities; glycoprotein levels including hexose, hexosamine, fucose, and sialic acid levels; and histone deacetylase activity as a cancer marker were determined. Oxidative stress markers were impaired and glycoprotein levels and histone deacetylase activity were increased in the D, C, and DC groups. Metformin therapy reversed these effects. Metformin was found to protect the brain and cerebellum of STZ-induced diabetic rats with Dunning prostate cancer from harm caused by MAT-Lylu metastatic cells.
Keyphrases
- diabetic rats
- oxidative stress
- prostate cancer
- papillary thyroid
- type diabetes
- squamous cell
- induced apoptosis
- nitric oxide
- radical prostatectomy
- white matter
- resting state
- small cell lung cancer
- dna damage
- cardiovascular disease
- ischemia reperfusion injury
- reactive oxygen species
- subarachnoid hemorrhage
- cerebral ischemia
- dendritic cells
- emergency department
- wound healing
- mesenchymal stem cells
- squamous cell carcinoma
- insulin resistance
- bone marrow
- young adults
- blood brain barrier
- multiple sclerosis
- gene expression
- drug induced
- uric acid
- high glucose
- high fat diet
- heat shock protein
- early stage
- cell death
- amino acid
- stem cells
- neoadjuvant chemotherapy
- diabetic nephropathy
- climate change
- fatty acid