Protective effect of sterubin against neurochemical and behavioral impairments in rotenone-induced Parkinson's disease.

This study was conducted to evaluate how sterubin affects rotenone-induced Parkinson's disease (PD) in rats. A total of 24 rats were distributed into 4 equal groups: normal saline control and rotenone control were administered saline or rotenone (ROT), respectively, orally; sterubin 10 received ROT + sterubin 10 mg/kg po; and sterubin alone was administered to the test group (10 mg/kg). Rats of the normal saline and sterubin alone groups received sunflower oil injection (sc) daily, 1 h after receiving the treatments cited above, while rats of the other groups received rotenone injection (0.5 mg/kg, sc). The treatment was continued over the course of 28 days daily. On the 29th day, catalepsy and akinesia were assessed. The rats were then euthanized, and the brain was extracted for estimation of endogenous antioxidants (MDA: malondialdehyde, GSH: reduced glutathione, CAT: catalase, SOD: superoxide dismutase), nitrative (nitrite) stress markers, neuroinflammatory cytokines, and neurotransmitter levels and their metabolites (3,4-dihydroxyphenylacetic acid (DOPAC), dopamine (DA), norepinephrine (NE), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA)). Akinesia and catatonia caused by ROT reduced the levels of endogenous antioxidants (GSH, CAT, and SOD), elevated the MDA level, and altered the levels of nitrites, neurotransmitters, and their metabolites. Sterubin restored the neurobehavioral deficits, oxidative stress, and metabolites of altered neurotransmitters caused by ROT. Results demonstrated the anti-Parkinson's activities of sterubin in ROT-treated rats.

Protective effect of sterubin against neurochemical and behavioral impairments in rotenone-induced Parkinson's disease

This study was conducted to evaluate how sterubin affects rotenone-induced Parkinson's disease (PD) in rats. A total of 24 rats were distributed into 4 equal groups: normal saline control and rotenone control were administered saline or rotenone (ROT), respectively, orally; sterubin 10 received ROT + sterubin 10 mg/kg po; and sterubin alone was administered to the test group (10 mg/kg). Rats of the normal saline and sterubin alone groups received sunflower oil injection (sc) daily, 1 h after receiving the treatments cited above, while rats of the other groups received rotenone injection (0.5 mg/kg, sc). The treatment was continued over the course of 28 days daily. On the 29th day, catalepsy and akinesia were assessed. The rats were then euthanized, and the brain was extracted for estimation of endogenous antioxidants (MDA: malondialdehyde, GSH: reduced glutathione, CAT: catalase, SOD: superoxide dismutase), nitrative (nitrite) stress markers, neuroinflammatory cytokines, and neurotransmitter levels and their metabolites (3,4-dihydroxyphenylacetic acid (DOPAC), dopamine (DA), norepinephrine (NE), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA)). Akinesia and catatonia caused by ROT reduced the levels of endogenous antioxidants (GSH, CAT, and SOD), elevated the MDA level, and altered the levels of nitrites, neurotransmitters, and their metabolites. Sterubin restored the neurobehavioral deficits, oxidative stress, and metabolites of altered neurotransmitters caused by ROT. Results demonstrated the anti-Parkinson's activities of sterubin in ROT-treated rats.

Fustin alleviates lipopolysaccharide-induced anxiety-depression-like performances by modulation of oxidative stress/neuroinflammatory markers/ NF-κB/caspase-3/BDNF expression in rodents.

OBJECTIVE: Anxiety and depression are common psychiatric disorders that affect millions of people worldwide. Lipopolysaccharide (LPS) is a bacterial endotoxin that has been demonstrated to cause depression and anxiety-like behaviors in animal models. Fustin is a flavonoid found in various plant species that have been reported to have neuroprotective effects. The study proposed the evaluation of fustin's impact on anxiety and depression in LPS-injected rats. MATERIALS AND METHODS: The efficacy of fustin in higher and lower doses was studied by administering a single dose of LPS-injected anxiety/depression in rodents. Behavioral models like the elevated plus maze test, open field test, marble burying test, force swimming test, tail suspension test, and hyperemotionality behavior were performed to evaluate anxiety/depression in rodents. The neuroinflammatory markers such as interleukin-6 (IL-6), interleukin-1ß (IL-1ß), nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), apoptosis marker caspase-3, and brain-derived neurotrophic factor (BDNF) were also measured as a part of the study. Additionally, biochemical markers of oxidative stress, such as malonaldehyde (MDA) and antioxidants, including superoxide dismutase (SOD), glutathione (GSH), catalase (CAT), and nitric oxide (NO), were also evaluated. RESULTS: LPS administration resulted in significant (p<0.001) changes in behavior tests and biochemical markers including IL-1ß, IL-6, NF-κB, TNF-α, NO, caspase-3, BDNF, MDA, CAT, SOD, and GSH. In contrast, treating the rats with fustin significantly improved the behavior tests and restored the changes in biochemical markers. CONCLUSIONS: The current work established the efficacy of fustin with its therapeutic impact on depression and anxiety-like behaviors in rodent experimental models through its modulation of apoptosis markers, oxidative stress, and neuroinflammation.