Brain research bulletin
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Brain research bulletin · Sep 2017
The effect of monascin on hematoma clearance and edema after intracerebral hemorrhage in rats.
Intracerebral hemorrhage (ICH) is a particularly devastating form of stroke with high mortality and morbidity. Hematomas are the primary cause of neurologic deficits associated with ICH. The products of hematoma are recognized as neurotoxins and the main contributors to edema formation and tissue damage after ICH. Finding a means to efficiently promote absorption of hematoma is a novel clinical challenge for ICH. Peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor erythroid 2-related factor 2 (Nrf2), had been shown that, can take potential roles in the endogenous hematoma clearance. However, monascin, a novel natural Nrf2 activator with PPARγ agonist, has not been reported to play a role in ICH. This study was designed to evaluate the effect of monascin on neurological deficits, hematoma clearance and edema extinction in a model of ICH in rats. ⋯ Our study demonstrated that the high dosage of monascin played a neuroprotective role in ICH through reducing BBB permeability, edema and hematoma volume.
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Brain research bulletin · Sep 2017
The protective effect of hydrogen sulfide (H2S) on traumatic brain injury (TBI) induced memory deficits in rats.
Traumatic brain injury (TBI), as an expanding public health epidemic, is a common cause of death among youth. TBI is associated with cognitive deficits and memory impairment. Hydrogen sulfide (H2S), a novel gaseous mediator, has been recognized as an important neuromodulator and neuroprotective agent in the central nervous system. ⋯ Treatment with NaHS (5 mg/kg) decreased the escape latency [F (1, 24)=7.559, P<0.05, two-way ANOVA] and traveled distance [F (1, 12)=6.398, P<0.05, Two way ANOVA)]. In probe test, injured animals spent less time in target zone (P<0.05, unpaired t-test) and NaHS did not have any effect on this parameter (p>0.05, one way ANOVA). These findings suggest that NaHS has a neuroprotective effect on TBI-induced memory impairment in rats.
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Brain research bulletin · May 2017
Neurogenic bladder dysfunction does not correlate with astrocyte and microglia activation produced by graded force in a contusion-induced spinal cord injury.
Rodent models for the study of neurogenic bladder dysfunction after spinal cord injury (SCI) are difficult to standardize, particularly when evaluating the specific contribution of the SCI to end-organ function. The purpose of this study was to evaluate the degree of bladder dysfunction associated with a highly reproducible, contusion-induced SCI in female rats. An infinite horizon impactor was used to create a contusion SCI with a magnitude of either 100 or 150 kDyne at the T8/T9 thoracic region of female Sprague-Dawley rats. ⋯ After performing the cystometric studies substantial differences were found in both SCI groups when compared to intact animals, specifically a high frequency of non-voiding contractions, different durations for intraluminal pressure-high frequency oscillations, intercontractile intervals, impaired micturition volumes, and estimated voiding efficiency. These results suggest that a contusion SCI can increase microglia and astrocyte activation without a strong association with bladder dysfunction. The present study will be important for precise considerations about correlating the intensity of an SCI with impairment outcomes at both locomotor or organ function levels.
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Brain research bulletin · May 2017
L-carnitine prevents memory impairment induced by chronic REM-sleep deprivation.
Sleep deprivation (SD) negatively impacts memory, which was related to oxidative stress induced damage. L-carnitine is a naturally occurring compound, synthesized endogenously in mammalian species and known to possess antioxidant properties. In this study, the effect of L-carnitine on learning and memory impairment induced by rapid eye movement sleep (REM-sleep) deprivation was investigated. ⋯ Furthermore, L-carnitine normalized chronic REM-sleep deprivation induced reduction in the hippocampus ratio of GSH/GSSG, activity of catalase, GPx, and SOD. No change was observed in TBARS among tested groups (P>0.05). In conclusion, chronic REM-sleep deprivation induced memory impairment, and treatment with L-carnitine prevented this impairment through normalizing antioxidant mechanisms in the hippocampus.
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Brain research bulletin · Apr 2017
Overexpression of phosphodiesterase-4 subtypes involved in surgery-induced neuroinflammation and cognitive dysfunction in mice.
Postoperative cognitive dysfunction (POCD) is characterized by cognitive impairments in patients after surgery. Hippocampal neuroinflammation induced by surgery is highly associated with POCD. Phosphodiesterase-4 (PDE4) is an enzyme that specifically hydrolyses cyclic adenosine monophosphate (cAMP), which plays an important role during neuroinflammation and the process of learning and memory. ⋯ Meanwhile, rolipram attenuated the cognitive impairment and the elevation of pro-inflammatory cytokines induced by surgery. Moreover, rolipram reversed the reduction of p-CREB and PSD95. These results indicate that PDE4 subtype overexpression may be involved in the development of surgery-induced cognitive dysfunction in mice.