Selenium attenuates apoptosis, inflammation and oxidative stress in the blood and brain of aged rats with scopolamine-induced dementia

Abstract

A potent antioxidant, selenium might modulate dementia-induced progression of brain and blood oxidative and apoptotic injuries. The present study explores whether selenium protects against experimental dementia (scopolamine, SCOP)-induced brain, and blood oxidative stress, apoptosis levels, and cytokine production in rats. Thirty-two rats were equally divided into four groups. The first group was used as an untreated control. The second group was treated with SCOP to induce dementia. The third and fourth groups received 1.5 mg/kg selenium (sodium selenite) and SCOP + selenium, respectively. Dementia was induced in the second and forth groups by intraperitoneal SCOP (1 mg/kg) administration. Brain, plasma, and erythrocyte lipid peroxidation levels as well as plasma TNF-α, interleukin (IL)-1β, and IL-4 levels were high in the SCOP group though they were low in selenium treatments. Selenium and selenium + SCOP treatments increased the lowered glutathione peroxidase activity, reduced glutathione, vitamins A and E concentrations in the brain, erythrocytes and plasma of the SCOP group. Apoptotic value expressions as active caspase-3, procaspase-9, and PARP were also increased by SCOP, while they were decreased by selenium and selenium + SCOP treatments. In conclusion, selenium induced protective effects against experimental dementia-induced brain, and blood oxidative injuries and apoptosis through regulation of cytokine production, vitamin E, glutathione concentrations, and glutathione peroxidase activity.

Hypericum perforatum L. supplementation protects sciatic nerve injury-induced apoptotic, inflammatory and oxidative damage to muscle, blood and brain in rats

“…[33] TNF-a and IL-1b are also responsible on neuronal apoptosis and inflammation in several neurological diseases such as dementia of Alzheimer's disease and injury of spinal cord. [20,34] Results of recent reports have indicated that proinflammatory cytokines including as TNF-a and IL-1a acted significant neuroprotective role in generation and maintenance of SNI, although TNF-a [35] and IL-1a [36] treatments evoke spontaneous firing of sciatic nerve. Antiinflammatory effect of HPL through inhibition of 5-lipoxygenase [37] and cytosolic phospholipase A2 [38] was reported.…”

“…The brain was also taken as follows; the cortex was dissected out after the brain was split in the mid‐sagittal plane. Following removal of the cortex, brain cortex was dissected from total brain . The soleus muscle samples from right legs were also taken.…”

“…IL‐1β (Wuhan Fine Biological Technological Co., Ltd, Wuhan, China), melatonin, IL‐2 and TNF‐α (DRG Inc., Marburg, Germany) and IL‐2 levels were measured using a manufacturer's enzyme‐linked immunosorbent assay, following the manufacturer's instructions . The absorbance of cytokines in the samples was read at 450 nm by Infinite pro200 microplate reader (Tecan Inc, Groedig, Austria), although absorbance of melatonin was read in the plate reader at 405 nm.…”

“…Following removal of the cortex, brain cortex was dissected from total brain. [20] The soleus muscle samples from right legs were also taken.…”

“…Cytokine and melatonin assays in plasma IL-1b (Wuhan Fine Biological Technological Co., Ltd, Wuhan, China), melatonin, IL-2 and TNF-a (DRG Inc., Marburg, Germany) and IL-2 levels were measured using a manufacturer's enzyme-linked immunosorbent assay, following the manufacturer's instructions. [20] The absorbance of cytokines in the samples was read at 450 nm by Infinite pro200 microplate reader (Tecan Inc, Groedig, Austria), although absorbance of melatonin was read in the plate reader at 405 nm. Determinations were made in duplicate, and IL-1b and TNF-a results are expressed in picogram (pg) per millilitre, although melatonin, IL-1b, TNF-a results are expressed in nanogram (ng) per millilitre.…”