Curcumin prevents neuronal loss and structural changes in the superior cervical (sympathetic) ganglion induced by chronic sleep deprivation, in the rat model.

BACKGROUND: In modern societies, sleep deprivation is a serious health problem. This problem could be induced by a variety of reasons, including lifestyle habits or neurological disorders. Chronic sleep deprivation (CSD) could have complex biological consequences, such as changes in neural autonomic control, increased oxidative stress, and inflammatory responses. The superior cervical ganglion (SCG) is an important sympathetic component of the autonomic nervous system. CSD can lead to a wide range of neurological consequences in SCG, which mainly supply innervations to circadian system and other structures. As the active component of Curcuma longa, curcumin possesses many therapeutic properties; including neuroprotective. This study aimed to evaluate the effect of CSD on the SCG histomorphometrical changes and the protective effect of curcumin in preventing these changes. METHODS: Thirty-six male rats were randomly assigned to the control, curcumin, CSD, CSD + curcumin, grid floor control, and grid floor + curcumin groups. The CSD was induced by a modified multiple platform apparatus for 21 days and animals were sacrificed at the end of CSD or treatment, and their SCGs removed for stereological and TUNEL evaluations and also spatial arrangement of neurons in this structure. RESULTS: Concerning stereological findings, CSD significantly reduced the volume of SCG and its total number of neurons and satellite glial cells in comparison with the control animals (P < 0.05). Treatment of CSD with curcumin prevented these decreases. Furthermore, TUNEL evaluation showed significant apoptosis in the SCG cells in the CSD group, and treatment with curcumin significantly decreased this apoptosis (P < 0.01). This decrease in apoptosis was observed in all control groups that received curcumin. CSD also changed the spatial arrangement of ganglionic neurons into a random pattern, whereas treatment with curcumin preserved its regular pattern. CONCLUSIONS: CSD could potentially induce neuronal loss and structural changes including random spatial distribution in the SCG neurons. Deleterious effects of sleep deprivation could be prevented by the oral administration of curcumin. Furthermore, the consumption of curcumin in a healthy person might lead to a reduction of cell death.

Beneficial Effects of Olive Oil on the Rats' Cerebellum: Functional and Structural Evidence.

BACKGROUND: Olive oil is a food additive and used in many biological studies as a solvent for other chemicals, including drugs. AIM: The present study aimed to investigate the effects of olive oil on rats' cerebellum structure and motor function. MATERIALS AND METHODS: Male rats were randomly divided into two groups orally receiving distilled water and olive oil (1 ml/kg/day). At the end of week 4, motor function was assessed in the rotarod test. The cerebellum was removed for stereo-logical assessment. Data were analyzed using a two-way repeated measures ANOVA for rotarod test and Kruskal-Wallis and Mann-Whitney U test for quantitative histological parameters. RESULTS: Performance of the olive oil-treated rats in fixed and accelerating speed rotarod was better and their riding time (endurance) was greater compared to the control group (p<0.05). However, no significant difference was found between the two groups regarding the total volume of the cerebellar hemisphere, its cortex, and deep cerebellar nuclei. The total number of the Purkinje, Bergman, and Golgi of the granular layer as well as neurons of the deep cerebellar nuclei was 26 - 36% higher in the olive oil-treated rats than in the distilled water treated group (p<0.03). CONCLUSION: The study findings suggest that olive oil has neuroprotective effects on the cerebellum and induces better performance of the rats in the rotarod.

Sodium benzoate, a food preservative, induces anxiety and motor impairment in rats.

OBJECTIVE: To investigate the behavioral characteristics, including anxiety and motor impairment, in sodium benzoate (NaB) treated rats. METHODS: The study was carried out between July and September 2012 in the Laboratory Animal Center of Shiraz University of Medical Sciences, Shiraz, Iran. The rats were divided into 2 groups receiving distilled water and NaB (200mg/kg/day). All the animals received daily gavages for 4 weeks. At the end of the fourth week, anxiety, and motor function were assessed in elevated plus maze and rotarod test. RESULTS: According to the results, NaB-treated rats spent less time in the open arm and had fewer entrances to the open arms in comparison with the control group (p<0.04). Also, the performance of the NaB-treated rats in fixed and accelerating speed rotarods was impaired, and the riding time (endurance) was lower than the control group (p<0.01). CONCLUSION: The performance of the NaB-treated rats was impaired in the elevated plus maze, an indicator of anxiety. Their riding time in fixed and accelerating speed rotarods was decreased, indicating motor impairment.

Curcumin mitigates the sleep-deprivation impacts on rat hypothalamic paraventricular nucleus.

Introduction: The paraventricular nucleus of the hypothalamus (PVH) is an important efferent system that relays the circadian rhythm of sleep and stress information to the periphery. Chronic REM sleep deprivation (CSD) is thought to damage this system. We evaluated the effects of CSD after 21 days on the spatial arrangement of PVH in male rats and the anti-apoptotic effects of curcumin on cell loss in sleep-deprived rats. Methods: The rats received 1 mL of 100 mg/kg/day of curcumin in 3 groups: the CSD (through a modified multiple platform apparatus, 18 h/day), grid-floor control, and cage-control along with the same set of matched groups which received 1 mL PBS. In the grid-floor control group, as a control for CSD, animals were placed on stainless-steel-mesh grids positioned upon the CSD apparatus and then allowed to sustain the chance to sleep. After 21 days, their brains were removed for stereological estimations, Voronoi tessellation, and TUNEL assay. In an unbiased stereological approach, Cavalieri's principle and an optical disector were used for estimating the volume and total cell number of the PVH, respectively. The Voronoi tessellation was measured using Image J software. Results: Significant reductions (P < 0.05) in the PVH volume and cell number, along with an increase in dead neurons, were found in CSD animals. The spatial pattern of two types of PVH neurons (parvocellular and magnocellular) showed random distributions after CSD, whereas curcumin not only increased the volume and neuronal number but also retrieved the spatial distribution to a regular one. Conclusions: CSD decreased the volume and altered the spatial arrangement of the neurons in PVH by increasing apoptosis and decreasing the cell number. However, oral use of curcumin could protect PVH from these changes.

The effects of copper sulfate on the structure and function of the rat cerebellum: A stereological and behavioral study.

Copper (Cu) is a vital trace element that acts as a cofactor of proteins and enzymes in many molecular pathways including the central nervous system. The accumulation or deficiency of copper could alter neuronal function and lead to neuronal degeneration and brain dysfunction. Intake of high levels of copper can also cause copper toxicosis that affects the brain structure and function. Despite clinical and experimental data indicating the association between abnormal copper homeostasis and brain dysfunction, the effects of copper on cerebellum have remained poorly understood. Hence, this study aimed to evaluate the effects of copper sulfate on the cerebellum via stereological and behavioral methods in rats. Male rats (Sprague-Dawley) were divided to three groups. The rats in the control group orally received distilled water, while those in the Cu groups received 1 mM (159 mg/L) or 8 mM (1272 mg/L) copper sulfate by oral gavage solved in distilled water daily for 4 weeks. Then, the rotarod performance test was recorded and the cerebellum was prepared for stereological assessments. The Cu-administered rats (1 and 8 mM) exhibited a significant reduction in the total volumes of the cerebellum structures. The total number of the cells in the cerebellar cortex and deep cerebellar nuclei were significantly decreased via Cu in a dose-dependent manner. Furthermore, the length of nerve fibers and the number of spines per nerve fiber decreased significantly in the Cu groups. These changes were correlated to the animals' motor performance impairment in the rotarod test. The findings suggested that copper toxicity induced motor performance impairments in the rats, which could be attributed to its deleterious effects on the cerebellum structure.

Spinal cord injury repair using mesenchymal stem cells derived from bone marrow in mice: A stereological study.

Transplantation of bone marrow stem cells (BMSCs) has shown to have a vital role in promoting nerve regeneration after SCI. The aim of this study was to investigate the effect of BMSCs transplantation in healing of spinal cord injury (SCI) in mice based on morphologic parameters. Forty two male mice were randomly divided into 3 groups of control with no intervention, experimental SCI without treatment, and experimental SCI transplanted with 2 × 105 BMSCs intravenously. To induce SCI bilaterally, T10 was compressed for 2 min. The animals were sacrificed 3 and 5 weeks after SCI and T7-T11 segments of spinal cord were removed and stained by Giemsa and H&E methods. Stereological assessment estimated the gray and white matter volume, the number of neurons and neuroglia and diameter of central canal. The average amount of gray matter in SCI injury group was significantly lower than control group. An increase in the number of neurons was noted after cell transplantation. The number of neurons in SCI injury group significantly decreased in comparison to the control group. In cell transplantation group, a significant increase in the number of neurons was visible when compared to SCI injury group. The increase in the number of neurons after cell transplantation denotes to the regenerative potential of BMSCs in SCI. These findings can be added to the literature and open a new window when targeting treatment of SCI.

Curcumin prevents neuronal loss and structural changes in the superior cervical (sympathetic) ganglion induced by chronic sleep deprivation, in the rat model

BACKGROUND: In modern societies, sleep deprivation is a serious health problem. This problem could be induced by a variety of reasons, including lifestyle habits or neurological disorders. Chronic sleep deprivation (CSD) could have complex biological consequences, such as changes in neural autonomic control, increased oxidative stress, and inflammatory responses. The superior cervical ganglion (SCG) is an important sympathetic component of the autonomic nervous system. CSD can lead to a wide range of neurological consequences in SCG, which mainly supply innervations to circadian system and other structures. As the active component of Curcuma longa, curcumin possesses many therapeutic properties; including neuroprotective. This study aimed to evaluate the effect of CSD on the SCG histomorphometrical changes and the protective effect of curcumin in preventing these changes. METHODS: Thirty-six male rats were randomly assigned to the control, curcumin, CSD, CSD + curcumin, grid floor control, and grid floor + curcumin groups. The CSD was induced by a modified multiple platform apparatus for 21 days and animals were sacrificed at the end of CSD or treatment, and their SCGs removed for stereological and TUNEL evaluations and also spatial arrangement of neurons in this structure. RESULTS: Concerning stereological findings, CSD significantly reduced the volume of SCG and its total number of neurons and satellite glial cells in comparison with the control animals ( P < 0.05). Treatment of CSD with curcumin prevented these decreases. Furthermore, TUNEL evaluation showed significant apoptosis in the SCG cells in the CSD group, and treatment with curcumin significantly decreased this apoptosis ( P < 0.01). This decrease in apoptosis was observed in all control groups that received curcumin. CSD also changed the spatial arrangement of ganglionic neurons into a random pattern, whereas treatment with curcumin preserved its regular pattern. CONCLUSIONS: CSD could potentially induce neuronal loss and structural changes including random spatial distribution in the SCG neurons. Deleterious effects of sleep deprivation could be prevented by the oral administration of curcumin. Furthermore, the consumption of curcumin in a healthy person might lead to a reduction of cell death.

Stereological studies of the effects of sodium benzoate or ascorbic acid on rats` cerebellum.

OBJECTIVES: To evaluate the cerebellar structure in sodium benzoate (NaB) or ascorbic acid (AA) treated rats. METHODS: This experimental study was conducted between May and September 2013 in the Laboratory Animal Center of Shiraz University of Medical Sciences, Shiraz, Iran. The rats received distilled either water, NaB (200mg/kg/day), AA (100mg/kg/day), or NaB+AA. The hemispheres were removed after 28 days and underwent quantitative study. RESULTS: The total volume of the cerebellar hemisphere, its cortex, intracerebellar nuclei; the total number of the Purkinje, Bergman, granule, neurons, and glial cells of the molecular layer; and neurons and glial cells of the intracerebellar nuclei reduced by 21-52% in the NaB-treated rats compared with the distilled water group (p=0.004). The total number of the Purkinje, Bergman, Golgi, and granule cells was 29-45% higher in the AA-treated rats compared with the distilled water group (p=0.05). However, these measures reduced by 17-50% in the NaB+AA-treated rats compared with the distilled water group (p=0.004). The NaB+AA group did not induce any significant structural changes in comparison with the NaB group (p>0.05). CONCLUSIONS: The NaB exposure with or without AA treatment could alter the cerebellum. Yet, AA could prevent the loss of some cells in the cerebellum. 

Effect of benzene on the cerebellar structure and behavioral characteristics in rats

Objective:To investigate the effects of benzene on rat’s cerebellum structure and behavioral characteristics, including anxiety and motor impairment. Methods:Twenty rats were randomly allocated into two groups orally receiving distilled water and benzene (200 mg/kg/day). A total of 10 rats were used at the beginning of benzene exposure. Two rats died during benzene treatment and 8 rats remained for evaluation of the behavioral test and finally 6 rats underwent histological assessment. At the end of the 4th week, motor function and anxiety were evaluated in rotarod test and elevated plus maze, respectively. Besides, the cerebellum was dissected for structural assessment using stereological methods. Results:Performance of the benzene-treated rats in fixed and accelerating speed rotarod was impaired and their riding time (endurance) was lower compared to the control group (P=0.02). The benzene-treated rats also spent less time in the open arms and had fewer entrances to the open arms in comparison to the control group, indicating anxiety (P=0.01). The total volume of the cerebellar hemisphere, its cortex, intracerebellar nuclei, total number of the Purkinje, Bergmann, Golgi, granule, neurons and glial cells of the molecular layer, and neurons and glial cells of the intracerebellar nuclei were reduced by 34%-76%in the benzene-treated rats in comparison to the distilled water group (P=0.003). The most cell loss was seen in Bergmann glia. Conclusions:The structure of cerebellum altered after benzene treatment. In addition, motor impairment and anxiety could be seen in benzene-treated rats.