Increased apoptosis, tumor necrosis factor‑α, and DNA damage attenuated by 3’,4’‑dihydroxyflavonol in rats with brain İschemia‑reperfusion
By: Dasdelen, Dervis
.
Contributor(s): Solmaz, Merve.
Publisher: Mumbai Wolter Kluwer 2021Edition: Vol.53(1), Jan-Feb.Description: 39-49p.Subject(s): PHARMACOLOGYOnline resources: Click here
In:
Indian Journal of PharmacologySummary: OBJECTIVES: This research was aimed to find out the effects of 3’,4’‑dihydroxyflavonol (DiOHF)
on apoptosis, DNA damage, and tumor necrosis factor‑α (TNF‑α) levels in the frontal cortex of rats
with induced experimental brain ischemi reperfusion.
MATERIALS AND METHODS: A total of 38 Wistar albino male rats were used. Groups were created as
1‑Sham; 2‑Ischemia‑reperfusion (I/R); 3‑I/R + DiOHF (10 mg/kg); 4‑Ischemia + DiOHF + reperfusion;
5‑DiOHF + I/R. I/R was performed by carotid artery ligation for 30 min in anesthesized animals.
Following experimental applications, blood samples were taken from anesthetized rats to obtain
erythrocyte and plasma. Later, the rats were killed by cervical dislocation, and frontal cortex samples
were taken and stored at − 80oC for the analysis.
RESULTS: In the ischemic frontal cortex tissue sections degenerate neuron numbers, Terminal
deoxynucleotidyl transferase‑dUTP nick end labeling (TUNEL) positive cell ratio and caspase‑3
positive cell ratio increased. Malondialdehyde, TNF‑α, and 8‑OHdG levels were increased in both
plasma and tissue in ischemia group, whereas tissue and erythrocyte glutathione levels were
significantly suppressed. However, these values were significantly reversed by DiOHF treatment.
CONCLUSION: The results of the study showed that I/R significantly increased apoptosis, TNF‑α,
and DNA damage in rats with brain I/R. However, 10 mg/kg intraperitoneal DiOHF treatment improved
deterioted parameters.
| Item type | Current location | Call number | Status | Date due | Barcode | Item holds |
|---|---|---|---|---|---|---|
Articles Abstract Database
|
School of Pharmacy Archieval Section | Not for loan | 2022-0858 |
OBJECTIVES: This research was aimed to find out the effects of 3’,4’‑dihydroxyflavonol (DiOHF)
on apoptosis, DNA damage, and tumor necrosis factor‑α (TNF‑α) levels in the frontal cortex of rats
with induced experimental brain ischemi reperfusion.
MATERIALS AND METHODS: A total of 38 Wistar albino male rats were used. Groups were created as
1‑Sham; 2‑Ischemia‑reperfusion (I/R); 3‑I/R + DiOHF (10 mg/kg); 4‑Ischemia + DiOHF + reperfusion;
5‑DiOHF + I/R. I/R was performed by carotid artery ligation for 30 min in anesthesized animals.
Following experimental applications, blood samples were taken from anesthetized rats to obtain
erythrocyte and plasma. Later, the rats were killed by cervical dislocation, and frontal cortex samples
were taken and stored at − 80oC for the analysis.
RESULTS: In the ischemic frontal cortex tissue sections degenerate neuron numbers, Terminal
deoxynucleotidyl transferase‑dUTP nick end labeling (TUNEL) positive cell ratio and caspase‑3
positive cell ratio increased. Malondialdehyde, TNF‑α, and 8‑OHdG levels were increased in both
plasma and tissue in ischemia group, whereas tissue and erythrocyte glutathione levels were
significantly suppressed. However, these values were significantly reversed by DiOHF treatment.
CONCLUSION: The results of the study showed that I/R significantly increased apoptosis, TNF‑α,
and DNA damage in rats with brain I/R. However, 10 mg/kg intraperitoneal DiOHF treatment improved
deterioted parameters.
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