Taxifolin as a novel therapeutic agent for epileptic seizures induced by caffeine-induced oxidative stress in rats.

BACKGROUND: Epilepsy is a severe neurological disease that results from excessive and/or synchronized neuronal activity in the brain, and oxidative stress plays a role in its pathogenesis. Taxifolin is a flavonoid that exhibits antioxidant activity. OBJECTIVES: To investigate the effects of taxifolin on caffeine-induced epileptic seizures in rats and reveal the role of antioxidant activity in antiepileptic therapy. MATERIAL AND METHODS: Forty rats were divided into 4 groups (n = 6/group): caffeine 300 mg/kg group (CG), taxifolin 50 mg/kg + caffeine 300 mg/kg group (TCG), 2 mg/kg diazepam + 300 mg/kg caffeine group (DCG), and a healthy group (HG). Taxifolin was given to the TCG, and diazepam was given to the DCG orally. One hour later, caffeine was injected intraperitoneally into the CG, TCG and DCG rats. The time between the caffeine injection and the contractions (the latency period) was determined. Animals were euthanized 1 h after caffeine injection, and brain tissues were biochemically examined for oxidants and antioxidants. RESULTS: Taxifolin and diazepam prolonged the latency period to a similar extent (p = 0.549), while taxifolin was more successful in preventing mortality. Taxifolin suppressed the caffeine-induced increase in myeloperoxidase, total oxidant status and oxidative stress index, and decreased total glutathione, superoxide dismutase and total antioxidant status more effectively than diazepam (p < 0.05). CONCLUSIONS: We showed the relationship between antioxidant activity and epilepsy treatment, and demonstrated that taxifolin may be useful for treating epilepsy.

Investigation of the effects of post-operative intraperitoneal, oral, and rectal phenytoin administration on colorectal anastomosis in rats.

BACKGROUND: Anastomotic leakage is the most feared complication after colonic anastomosis. The purpose of the study is to determine the effects of phenytoin applied by different application routes, on the healing process of colorectal anastomoses. METHODS: Wistar Albino rats were divided into Intraperitoneal Phenytoin Group, Oral Phenytoin Group (OAP), Rectal Phenytoin Group (RAP), and control groups. The molecular effect of phenytoin on the expression of vascular endothelial growth factor (VEGF), transforming growth factor-beta (TGF-ß), fibroblast growth factor 2 (FGF2), and p53 genes was evaluated at mRNA and protein level. The effects of phenytoin on anastomotic bursting pressure analysis measured as well as pathohistological examinations. RESULTS: There are statistically significant increase in anastomotic bursting pressure values between control and application groups. Inflammatory cell infiltration of all groups increased in the intestinal anastomosis region compared to control. Collagen scores were found to be significantly higher in the OAP and RAP groups compared to the control group. mRNA of TGF-ß and FGF2 expression increased in all routes of phenytoin applications. CONCLUSION: Three different administration routes show considerably increase on the bursting pressure. Regarding the results of the expression of FGF2, TGF-ß, p53, and VEGF genes, there is a significant increase FGF2 and TGF-ß at mRNA and protein level in most administration routes.

Trigger Point Injection as a Rare Cause of Ischemic Stroke: A Case Report.

INTRODUCTION: Myofascial pain syndrome is a painful local or regional disease caused by myofascial trigger points. Trigger point injection (TPI) is a frequently used method for the treatment of myofascial pain. Major complications associated with TPI have rarely been reported in the literature. CASE REPORT: A 24-year-old woman, without medical history of any disease, was diagnosed with myofascial syndrome based on the presence of long-standing neck and right arm pain, and TPI with lidocaine was applied to the right trapezius region. During the procedure, blurred vision and loss of strength in the left arm occurred. Magnetic resonance and computed tomography imaging of the brain revealed findings that were consistent with an ischemic stroke in the right capsular interna and right occipital region. CONCLUSION: The reported patient is the first in the literature who suffered from ischemic stroke after TPI. The use of ultrasound for injections into the neck muscles could avoid serious complications.

Is ischemia associated with the formation of White matter lesions in migraine?

OBJECTIVE: White matter lesions (WMLs) are more common in migraine patients than in the normal population. Ischemia/hypoxia and oxidative stress are considered to play a role in WMLs formation. This study aimed to investigate ischemia-modified albumin (IMA), ferroxidase and thiol/disulfide homeostasis in migraineurs with and without WMLs. PATIENTS AND METHODS: Sixty-two migraineurs with WML, 59 migraineurs without WML and 61 controls were included in the study. All participants underwent brain MRI. WMLs was evaluated according to the Fazekas scale. IMA, ferroxidase, total thiol, native thiol and disulfide measurements were carried out in all participants. RESULTS: The IMA levels were higher in the migraine groups compared to the control group (p < 0.001) and in the WML group compared to non-WML (p < 0.001). The total and native thiol levels were higher in the non-WML group compared to the control and WML groups (p < 0.001 for both). The disulfide levels were similar between the control and non-WML groups, but they were significantly lower in the WML group compared to the control and non-WML groups. There was no significant difference between the groups in terms of the ferroxidase levels (p = 0.092). The thiol/disulfide, IMA and ferroxidase levels were not significantly correlated with the frequency and duration of attacks, severity of pain and disability due to migraine. CONCLUSION: Increased serum IMA levels in migraineurs point to the role of ischemia/hypoxia, and increased total thiol and decreased disulfide levels indicate an oxidant/antioxidant imbalance in migraine. Ischemia/hypoxia may play a role in WMLs formation in migraine.

Peripheral neurotoxic effects of cisplatin on rats and treatment with rutin.

BACKGROUND: Cisplatin, used in cancer treatment, has toxic and apoptotic effects on the peripheral nervous system. Rutin, also known as vitamin P, has antioxidant and antiapoptotic activity. OBJECTIVES: The purpose of this study was to investigate the biochemical and histopathologic efficacy of rutin on neurotoxic and apoptotic effects caused by cisplatin in the peripheral nervous system. MATERIAL AND METHODS: Twenty-four albino Wistar male rats were divided into the following 4 groups: control group (CG), only cisplatin-injected group (CIS), cisplatin and rutin 50 mg/kg (RG-50)-injected group, and cisplatin and rutin 100 mg/kg (RG-100)-injected group. Analyses were performed on sciatic nerve tissue of experimental animals. Analyses of malondialdehyde (MDA), total glutathione (tGSH), glutathione reductase (GSHRd), glutathione-s-transferase (GST), and superoxide dismutase (SOD) were performed. Caspase-3 expression in nerve tissue was also investigated. The analyzed groups were compared with CG. RESULTS: Biochemical investigation shows that there is a statistically significant difference between CG and only CIS and RG-50. Control group and RG-100 were found to be similar. Cisplatin-induced changes were observed in histopathological analysis of the nerve tissue. The RG-100 and CG were found to be similar. The caspase-3 expression in the neural tissue was compared between groups. Control group and CIS were found to be different. Control group and RG-100 were found to be similar. CONCLUSIONS: Antioxidant and antiapoptotic effectiveness of rutin was detected against the toxic effects caused by cisplatin in the peripheral nerve tissue.