Metformin treatment confers protection of the optic nerve following photoreceptor degeneration / 대한해부학회지

Acquired or inherited or photoreceptor loss causes retinal ganglion cell loss and ultimately axonal transport alteration. Thus, therapies should be applied early during photoreceptors degeneration before the remodeling process reaches the inner retina. This study aimed to evaluate the protective effect of metformin on the rat optic nerve following photoreceptors loss induced by N-Ethyl-N-nitrosourea (ENU). Eighteen adults male Wistar rats were divided into two groups. Group I: normal vehicle control (n=6). Group II: ENU-induced photoreceptors degeneration (n=12) received a single intraperitoneal injection of ENU at a dose of 600 mg/kg. Rats in group II were equally divided into two subgroups:IIa: photoreceptor degeneration induced group and IIb: metformin treated group (200 mg/kg) for 7 days. Specimens from the optic nerve were processed for light and electron microscopy. In ENU treated group, the optic nerve revealed reduction in the diameter of the optic nerve fibers and thinning of myelin sheath with morphological changes in the glia (astrocytes, oligodendrocytes, and microglia). Caspase-3 (apoptotic marker), iNOS (oxidative stress marker) and CD68 (macrophage marker) expression increased. In metformin-treated group, the diameter of optic nerve fibers and myelin sheath thickness increased with improvement of the deterioration in the glia. Caspase-3, iNOS and CD68 expression decreased. Metformin ameliorates the histological changes of the rat optic nerve following photoreceptors loss induced by ENU.

Metformin treatment confers protection of the optic nerve following photoreceptor degeneration / 대한해부학회지

Acquired or inherited or photoreceptor loss causes retinal ganglion cell loss and ultimately axonal transport alteration. Thus, therapies should be applied early during photoreceptors degeneration before the remodeling process reaches the inner retina. This study aimed to evaluate the protective effect of metformin on the rat optic nerve following photoreceptors loss induced by N-Ethyl-N-nitrosourea (ENU). Eighteen adults male Wistar rats were divided into two groups. Group I: normal vehicle control (n=6). Group II: ENU-induced photoreceptors degeneration (n=12) received a single intraperitoneal injection of ENU at a dose of 600 mg/kg. Rats in group II were equally divided into two subgroups:IIa: photoreceptor degeneration induced group and IIb: metformin treated group (200 mg/kg) for 7 days. Specimens from the optic nerve were processed for light and electron microscopy. In ENU treated group, the optic nerve revealed reduction in the diameter of the optic nerve fibers and thinning of myelin sheath with morphological changes in the glia (astrocytes, oligodendrocytes, and microglia). Caspase-3 (apoptotic marker), iNOS (oxidative stress marker) and CD68 (macrophage marker) expression increased. In metformin-treated group, the diameter of optic nerve fibers and myelin sheath thickness increased with improvement of the deterioration in the glia. Caspase-3, iNOS and CD68 expression decreased. Metformin ameliorates the histological changes of the rat optic nerve following photoreceptors loss induced by ENU.

Effect of acute pentylenetetrazol injection induced epileptic seizures on rat dentate gyrus at different postnatal ages / 대한해부학회지

Epilepsy is one of the most common neurological disorders, its prevalence approximately from 0.5% to 2% of the general population. Generalized seizures could lead to several morphological changes in the brain. This study aimed to investigate the morphological effects of a single convulsive dose of pentylenetetrazol (PTZ) on rat dentate gyrus at different postnatal ages. Thirty-six male Wistar rats were used at the following postnatal ages: P10, P21, and P90 (12 rats per each age). The animals in each age were equally divided into two groups: group I, control and group II, treated with a single intraperitoneal injection of PTZ (55 mg/kg). After confirmation of generalized tonic-clonic seizures, specimens from the right dentate gyrus were processed for light and electron microscopy. In PTZ-treated groups, the number of granule cells significantly decreased. Dark granule cells appeared in the deep layers of the granule cells in P10 and with the progress of age, they significantly increased in number and extended into the superficial layers of the granule cells. The dendritic spines diminished. Glial fibrillary acidic protein and caspase-3 expression increased. Ultrastructurally, granule cells showed irregular shaped nucleus, dilated rough endoplasmic reticulum (RER) cisternae, mitochondria with damaged cristae, large vacuoles, lysosomes, and lipofuscin granules. Dark granule cells characterized by electron-dense nucleus and cytoplasm containing disorganized Golgi bodies, swollen mitochondria with damaged cristae, numerous free ribosomes and few long strands of RER. Astrocytes had hypertrophied cell body. Acute treatment with PTZ-induced epileptic seizures caused toxic effect on the structure of rat dentate gyrus at different postnatal ages.

Effect of acute pentylenetetrazol injection induced epileptic seizures on rat dentate gyrus at different postnatal ages / 대한해부학회지

Epilepsy is one of the most common neurological disorders, its prevalence approximately from 0.5% to 2% of the general population. Generalized seizures could lead to several morphological changes in the brain. This study aimed to investigate the morphological effects of a single convulsive dose of pentylenetetrazol (PTZ) on rat dentate gyrus at different postnatal ages. Thirty-six male Wistar rats were used at the following postnatal ages: P10, P21, and P90 (12 rats per each age). The animals in each age were equally divided into two groups: group I, control and group II, treated with a single intraperitoneal injection of PTZ (55 mg/kg). After confirmation of generalized tonic-clonic seizures, specimens from the right dentate gyrus were processed for light and electron microscopy. In PTZ-treated groups, the number of granule cells significantly decreased. Dark granule cells appeared in the deep layers of the granule cells in P10 and with the progress of age, they significantly increased in number and extended into the superficial layers of the granule cells. The dendritic spines diminished. Glial fibrillary acidic protein and caspase-3 expression increased. Ultrastructurally, granule cells showed irregular shaped nucleus, dilated rough endoplasmic reticulum (RER) cisternae, mitochondria with damaged cristae, large vacuoles, lysosomes, and lipofuscin granules. Dark granule cells characterized by electron-dense nucleus and cytoplasm containing disorganized Golgi bodies, swollen mitochondria with damaged cristae, numerous free ribosomes and few long strands of RER. Astrocytes had hypertrophied cell body. Acute treatment with PTZ-induced epileptic seizures caused toxic effect on the structure of rat dentate gyrus at different postnatal ages.

Histological study on the effect of nicotine on adult male guinea pig thin skin / 대한해부학회지

Tobacco smoking has been identified as an important factor in premature skin aging to detect the histological changes occurred in adult male guinea pig thin skin under the influence of low and high doses of nicotine; which constitutes approximately 0.6%–3.0% of the dry weight of tobacco. Fifteen adult male pigmented guinea pigs were equally divided into three groups: group I, control; group IIA, low dose nicotine treated; 3 mg/kg subcutaneously for 4 weeks; and group IIB, high dose nicotine treated; 6 mg/kg subcutaneously for 4 weeks. Specimens from the back thin skin were processed for light and electron microscopy. Nicotine administration revealed flattened dermo-epidermal junction and reduced rete ridges formation. Collagen bundles were disorganized with increased spaces between them. A reduction in the amount of elastic fibers in the dermis were also observed compared to group I. Ultrastructurally, keratinocytes had hyperchromatic nuclei, intracytoplasmic vacuoles, disruption of desmosomal junctions, irregular tonofilaments distribution, and increased inter-cellular spaces. These changes were more pronounced with high dose nicotine administration. The epidermal thickness was reduced in low dose nicotine administration. But, high dose nicotine administration revealed increased epidermal thickness compared to the control group. Nicotine induced structural changes of adult male guinea pig thin skin. These changes were more pronounced with high dose nicotine administration.

Histological study on the effect of low level perinatal lead exposure on the cerebellar cortex of adult male albino rat

Lead contaminating drinking water is most often a problem in houses. As the nervous system is the primary target for the low levels of lead exposure, more attention has been directed towards lead poisoning. To determine the toxic effect of chronic low level of lead acetate on the histological structure of the cerebellar cortex of adult male albino rats. A total number of 5 pregnant albino rats were used. Lead exposure was initiated on gestation day 6 with the addition of daily doses of 0.2% lead acetate to distilled deionized drinking water and lasted until weaning. Half of the weaned male offspring were maintained on lead treated water supply until the age of two months [treated]. The remaining half received distilled deionized water until the age of 2 months [withdrawal]. Control animals received distilled deionized water. Specimens from the cerebellar cortex were processed for examination by light and electron microscope. Lead level in blood, urine and cerebellar tissue was estimated by spectrophotometry. In lead exposed rats, Purkinje cells, oligodendrocytes and Golgi cells were affected. The number of Purkinje cells decreased. The myelinated axons showed vacuoles. Blood capillaries were affected. Lead level in blood and cerebellar tissue was high. In the withdrawal group, some Purkinje cells revealed partial recovery while others showed more progress in degeneration. Chronic low level perinatal lead exposure had toxic effect on the cerebellar cortex of adult male albino rat mild regression was revealed after lead cessation