Histological and electroencephalographic demonstration of probiotic effect for reduce of oxidative stress and apoptosis in experimental traumatic brain injury.

BACKGROUND: The gut microbiota modulates nervous system function. In the literature, it has been shown that this modula-tion is used in many nervous system injuries through oxidative stress (OS) and apoptosis mechanisms. In this study, it was aimed to investigate the neuroprotective effects of probiotic (PB) treatment in a rat traumatic brain injury (TBI) model with histological and electroencephalographic (EEG) data. METHODS: Forty male Wistar albino rats were divided into four groups. Group 1 was the control group (CONTROL, n=10) and no trauma was applied. Group 2 was the trauma group with the weight-drop technique (TBH, n=10). Group 3 was the sham group (SHAM), (TBH+sterile saline [SS], n=10) rats were given 500 µL of SS per day by oral gavage. Group 4 was the PB treatment group, (TBH+PB, n=10) rats were treated daily for 7 days with 500 µL of PB oral gavage. Brain samples were collected 7 days after trauma. Histopathological evaluation of brain samples was done with HE. OS with Endothelial nitric oxide synthase, vascularization with Vas-cular Endothelial Growth Factor, gliosis with S100, and apoptosis with caspase 3 were evaluated immunohistochemically. Apoptotic index was determined with TUNEL. In addition, EEG and somatosensory evoked potential (SEP) recording findings were compared. RESULTS: It was determined by HE staining that there was a significant (P<0.001) damage in the TBI and sham groups compared to the control group. It was found that PB treatment provided a significant (P<0.01) improvement in the damage created. While OS (P<0.01), gliosis (P<0.01), and apoptosis (P<0.05) decreased with PB treatment, angiogenesis (P<0.01) increased. In support of these findings, in the software-mediated EEG and SUP examination; Delta wave power and theta/alpha ratio increased with TBI and de-creased with PB treatment. CONCLUSION: The results showed that PB treatment provided a significant improvement in rats by reducing OS, apoptosis, and gliosis and increasing vascularity. To the best of our knowledge in the literature, it was shown for the 1st time that histological results for the treatment of PB were supported by software-mediated EEG and SEP analysis.

Classical heart rate variability and nonlinear heart rate analysis in mice under Napentobarbital and ketamine/xylazine anesthesia.

BACKGROUND: Anesthetics are often used in animal experiments to achieve immobilization and relieve pain. However, many anesthetics can alter the dynamics of cardiovascular systems. We aimed to compare the effects of two frequently used anesthetics agents on heart rate variability (HRV) parameters in mice. METHODS: This observational study was performed between May and June 2014 in 21 male BALB/c mice aged 16-20 weeks. The animals were divided into three groups: pentobarbital (P), (n = 7); pentobarbital+fentanyl (P+F), (n = 7); and ketamine+xylazine (K+X), (n = 7). Surface electrocardiography (ECG) electrodes were placed in lead II configuration. The tachogram of RR intervals was obtained after R waves were detected using the Pan-Tompkins real-time QRS recognition algorithm. Frequency-domain, time-domain, and nonlinear HRV analyses were performed. RESULTS: The bradycardia effect was higher in the K+X group (p < 0.01). Time-domain indices were higher in group K+X compared to group P (p < 0.01) and group P+F (p < 0.001). Very low frequency (VLF) power was significantly lower in group K+X compared to group P and group P+F (p < 0.01). Low frequency (LF) power, low frequency/high frequency (LF/HF) ratio, and total power (TP) were higher in group K+X compared to group P (p < 0.01) and group P+F (p < 0.001). The detrended fluctuation analysis short-term parameter (DFAα1 ) was significantly higher in group K+X compared to group P+F (p < 0.05) and the long-term parameter (DFAα2 ) was lower in group K+X compared to group P (p < 0.05). Standard deviations SD1 and SD2 were higher in group K+X compared to group P (p < 0.001) and group P+F (p < 0.001), SD2/SD1 ratio was lower in group K+X compared to group P (p < 0.05) and group P+F (p < 0.05). Entropy measures did not differ between groups. DISCUSSION: HRV analyses, including nonlinear methods, indicated that a K+X combination reduces imbalance and disorder in the regulation of the autonomic nervous system (ANS) in comparison to both P and the P+F combination.

Therapeutic effects of Lacosamide in a rat model of traumatic brain injury: A histological, biochemical and electroencephalography monitoring study.

OBJECTIVE: Traumatic Brain Injury (TBI) is a major cause of death and disability worldwide, especially in children and young adults. TBI can be classified based on severity, mechanism or other features. Inflammation, apoptosis, oxidative stress, and ischemia are some of the important pathophys-iological mechanisms underlying neuronal loss after TBI. Lacosamide (LCM) is an anticonvulsant compound approved for the adjunctive treatment of partial-onset seizures and neuropathic pain. This study aimed to investigate possible neuroprotective effects of LCM in a rat model of TBI. MATERIAL AND METHODS: Twenty-eight adult male, Wistar albino rats were used. The rats were divided into 4 groups. Group 1 was the control group (n=7). Group 2 was the trauma group (n=7) where rats were treated with 100 mg/kg saline intraperitoneally (IP) twice a day. Groups 3 and 4, rats were treated with 6 (group 3, n=7) or 20 (group 4, n=7) mg/kg Lacosamide IP twice a day. For each group, brain samples were collected 72 hours after injury. Brain samples and blood were evaluated with histopathological and biochemical methods. In addition, electroencephalograpy monitoring results were compared. RESULTS: The immunoreactivity of both iNOS and eNOS (oxidative stress markers) were decreased with LCM treatment compared to trauma group. The results were statistically significant (***P<0.001). The treatments of low (56,17±9,69) and high-dose LCM (43,91±9,09) were decreased the distribution of HIF-1α compared to trauma group (P<0.01). The number of apoptotic cells were decreased with LCM treatment the difference between the trauma group and 20mg/kg LCM treated group (9,55±1,02) was statistically significant (***P<0.001). Malondialdehyde level was reduced with LCM treatment. MDA level was significantly higher in trauma group compared to LCM treated groups (***P<0.001). The level of Superoxide dismutase in the trauma group was 1,86 U/ml, whereas it was 36,85 U/ml in 20mg/kg LCM treated group (***P<0.001). Delta strength of EEG in 20mg/kg LCM treated group were similar to control group values after LCM treatment. CONCLUSION: No existing study has produced results suggesting that different doses of LCM has therapeutic effect against TBI, using EEG recording in addition to histological and biochemical evaluations in rats.