Background: Astrocytes have been implicated as potentially exerting both neurotoxic and neuroprotective activities in Parkinson’s disease. (Maragakis and Rothstein, 2006). Typically, astrocytes respond to brain tissue changes (whether it be due to injury, infection, or disease) by undergoing astrogliosis, a process involving the upregulation of the intermediate filament protein glial fibrillary acidic protein (GFAP), cell body enlargement, and proliferation (Sofroniew, Vinters, 2010). Conclusion: Our results demonstrate that oxidative stress and mitochondrial dysfunction involve nigral cellular elements other than dopaminergic neurons. These include astrocytes, microglia, vascular endothelial cells and pericytes which promote damage to the neurons.

Background: Astrocytes have been implicated as potentially exerting both neurotoxic and neuroprotective activities in Parkinson’s disease. (Maragakis and Rothstein, 2006). Typically, astrocytes respond to brain tissue changes (whether it be due to injury, infection, or disease) by undergoing astrogliosis, a process involving the upregulation of the intermediate filament protein glial fibrillary acidic protein (GFAP), cell body enlargement, and proliferation (Sofroniew, Vinters, 2010). Conclusion: Our results demonstrate that oxidative stress and mitochondrial dysfunction involve nigral cellular elements other than dopaminergic neurons. These include astrocytes, microglia, vascular endothelial cells and pericytes which promote damage to the neurons.

Background: Astrocytes have been implicated as potentially exerting both neurotoxic and neuroprotective activities in Parkinson’s disease. (Maragakis and Rothstein, 2006). Typically, astrocytes respond to brain tissue changes (whether it be due to injury, infection, or disease) by undergoing astrogliosis, a process involving the upregulation of the intermediate filament protein glial fibrillary acidic protein (GFAP), cell body enlargement, and proliferation (Sofroniew, Vinters, 2010). Conclusion: Our results demonstrate that oxidative stress and mitochondrial dysfunction involve nigral cellular elements other than dopaminergic neurons. These include astrocytes, microglia, vascular endothelial cells and pericytes which promote damage to the neurons.

Oxidative stress and inflammation are involved in the development and progression of diabetes and its complications. The renin–angiotensin system also plays an important role in the pathogenesis of diabetes and its complications. We hypothesized that curcumin and captopril would restore the kidney and nerve functions of diabetic rats through their angiotensin converting enzyme 1 (ACE1) inhibiting activity as well as their antioxidant and anti-inflammatory effects. Diabetes was induced by a single intraperitoneal injection of streptozotocin (100 mg·kg–1 body weight). One week after induction of diabetes, rats were treated with 100 mg·kg–1·day–1 curcumin or 50 mg·kg–1·day–1 captopril orally for 6 weeks. Compared with diabetic control rats, curcumin- or captopril-treated diabetic rats had significantly improved blood glucose, lipid profile, kidney/body weight ratio, serum creatinine, blood urea nitrogen (BUN), and pain thresholds assessed by Von Frey filaments, hot plate test, and tail-flick test. Diabetic control rats showed increased levels of total peroxide, renal and neural tumor necrosis factor-α and interleukin-10, and renal ACE1 compared with nondiabetic rats. Although treatment with either curcumin or captopril restored the altered variables, captopril was more effective in reducing these variables. ACE1 was positively correlated with BUN and creatinine and negatively correlated with paw withdrawal threshold, hot plate reaction time, and tail-flick latency, suggesting a possible causal relationship. We conclude that curcumin and captopril protect against diabetic nephropathy and neuropathy by inhibiting ACE1 as well as oxidation and inflammation. These findings suggest that curcumin and captopril may have a role in the treatment of diabetic nephropathy and neuropathy.

Oxidative stress and inflammation are involved in the development and progression of diabetes and its complications. The renin–angiotensin system also plays an important role in the pathogenesis of diabetes and its complications. We hypothesized that curcumin and captopril would restore the kidney and nerve functions of diabetic rats through their angiotensin converting enzyme 1 (ACE1) inhibiting activity as well as their antioxidant and anti-inflammatory effects. Diabetes was induced by a single intraperitoneal injection of streptozotocin (100 mg·kg–1 body weight). One week after induction of diabetes, rats were treated with 100 mg·kg–1·day–1 curcumin or 50 mg·kg–1·day–1 captopril orally for 6 weeks. Compared with diabetic control rats, curcumin- or captopril-treated diabetic rats had significantly improved blood glucose, lipid profile, kidney/body weight ratio, serum creatinine, blood urea nitrogen (BUN), and pain thresholds assessed by Von Frey filaments, hot plate test, and tail-flick test. Diabetic control rats showed increased levels of total peroxide, renal and neural tumor necrosis factor-α and interleukin-10, and renal ACE1 compared with nondiabetic rats. Although treatment with either curcumin or captopril restored the altered variables, captopril was more effective in reducing these variables. ACE1 was positively correlated with BUN and creatinine and negatively correlated with paw withdrawal threshold, hot plate reaction time, and tail-flick latency, suggesting a possible causal relationship. We conclude that curcumin and captopril protect against diabetic nephropathy and neuropathy by inhibiting ACE1 as well as oxidation and inflammation. These findings suggest that curcumin and captopril may have a role in the treatment of diabetic nephropathy and neuropathy.

Thyroid hormones and omega-3 are essential for normal brain functions. Recent studies have suggested that omega-3 may protect against the risk of dementia. The aim of this study was to investigate the effect of hypothyroidism on spatial learning and memory in adult male rats, the underlying mechanisms and the possible therapeutic value of omega-3 supplementation. Thirty male rats were divided into three groups; control, hypothyroid and omega-3 treated. Hypothyroidism induced significant deficits in working and reference memories in radial arm maze, retention deficits in passive avoidance test and impaired intermediate and long-term memories in novel object recognition test. Serum total antioxidant capacity (TAC) and hippocampal serotonin and γ-aminobutyric acid (GABA) levels were decreased in the hypothyroid group as compared to the control group. Moreover, the hippocampus of hypothyroid rats showed marked structural changes as diffuse vacuolar degeneration and distortion of the pyramidal cells. Immunohistochemistry showed that the expression of Cav1.2 (the voltage dependent LTCC alpha 1c subunit) protein was increased in the hypothyroid group as compared to the control group. Omega-3 supplementation ameliorated memory deficits, increased TAC, decreased the structural changes and decreased the expression of Cav1.2 protein. In conclusion omega-3 could be useful as a neuroprotective agent against hypothyroidism-induced cognitive impairment.

Thyroid hormones and omega-3 are essential for normal brain functions. Recent studies have suggested that omega-3 may protect against the risk of dementia. The aim of this study was to investigate the effect of hypothyroidism on spatial learning and memory in adult male rats, the underlying mechanisms and the possible therapeutic value of omega-3 supplementation. Thirty male rats were divided into three groups; control, hypothyroid and omega-3 treated. Hypothyroidism induced significant deficits in working and reference memories in radial arm maze, retention deficits in passive avoidance test and impaired intermediate and long-term memories in novel object recognition test. Serum total antioxidant capacity (TAC) and hippocampal serotonin and γ-aminobutyric acid (GABA) levels were decreased in the hypothyroid group as compared to the control group. Moreover, the hippocampus of hypothyroid rats showed marked structural changes as diffuse vacuolar degeneration and distortion of the pyramidal cells. Immunohistochemistry showed that the expression of Cav1.2 (the voltage dependent LTCC alpha 1c subunit) protein was increased in the hypothyroid group as compared to the control group. Omega-3 supplementation ameliorated memory deficits, increased TAC, decreased the structural changes and decreased the expression of Cav1.2 protein. In conclusion omega-3 could be useful as a neuroprotective agent against hypothyroidism-induced cognitive impairment.

Thyroid hormones and omega-3 are essential for normal brain functions. Recent studies have suggested that omega-3 may protect against the risk of dementia. The aim of this study was to investigate the effect of hypothyroidism on spatial learning and memory in adult male rats, the underlying mechanisms and the possible therapeutic value of omega-3 supplementation. Thirty male rats were divided into three groups; control, hypothyroid and omega-3 treated. Hypothyroidism induced significant deficits in working and reference memories in radial arm maze, retention deficits in passive avoidance test and impaired intermediate and long-term memories in novel object recognition test. Serum total antioxidant capacity (TAC) and hippocampal serotonin and γ-aminobutyric acid (GABA) levels were decreased in the hypothyroid group as compared to the control group. Moreover, the hippocampus of hypothyroid rats showed marked structural changes as diffuse vacuolar degeneration and distortion of the pyramidal cells. Immunohistochemistry showed that the expression of Cav1.2 (the voltage dependent LTCC alpha 1c subunit) protein was increased in the hypothyroid group as compared to the control group. Omega-3 supplementation ameliorated memory deficits, increased TAC, decreased the structural changes and decreased the expression of Cav1.2 protein. In conclusion omega-3 could be useful as a neuroprotective agent against hypothyroidism-induced cognitive impairment.

Thyroid hormones and omega-3 are essential for normal brain functions. Recent studies have suggested that omega-3 may protect against the risk of dementia. The aim of this study was to investigate the effect of hypothyroidism on spatial learning and memory in adult male rats, the underlying mechanisms and the possible therapeutic value of omega-3 supplementation. Thirty male rats were divided into three groups; control, hypothyroid and omega-3 treated. Hypothyroidism induced significant deficits in working and reference memories in radial arm maze, retention deficits in passive avoidance test and impaired intermediate and long-term memories in novel object recognition test. Serum total antioxidant capacity (TAC) and hippocampal serotonin and γ-aminobutyric acid (GABA) levels were decreased in the hypothyroid group as compared to the control group. Moreover, the hippocampus of hypothyroid rats showed marked structural changes as diffuse vacuolar degeneration and distortion of the pyramidal cells. Immunohistochemistry showed that the expression of Cav1.2 (the voltage dependent LTCC alpha 1c subunit) protein was increased in the hypothyroid group as compared to the control group. Omega-3 supplementation ameliorated memory deficits, increased TAC, decreased the structural changes and decreased the expression of Cav1.2 protein. In conclusion omega-3 could be useful as a neuroprotective agent against hypothyroidism-induced cognitive impairment.

Obesity can be associated with dysfunction of the immune system. An increased risk of obesity has been reported among individuals with low levels of vitamin D. However, much is still unknown about the link between vitamin D and dysfunction of the spleen and immune system in obesity. Therefore, the objectives of this study were to evaluate the effects of a high-fat diet (HFD) on the spleen and immune system and to determine the protective effects of chronic treatment with vitamin D in reversing the detrimental effects of HFD. Body weight (BW) gain, the serum levels of calcium, C-reactive protein (CRP), and interleukin-10 (IL-10), and the expression of both CD86 and caspase-3 in the spleen were investigated. Twenty-four adult male Wistar rats were divided into three equal groups: the control (C) group received a control diet for 10 weeks, the HFD-C group received a HFD for 10 weeks, and the HFD-treated group received a HFD co-administered with oral vitamin D (1 μg/kg) daily for 10 weeks. Administration of vitamin D in combination with HFD significantly decreased BW gain, decreased the serum levels of both calcium and CRP, increased the serum level of IL-10, improved the general histological appearance of the spleen, and decreased the expression of both CD86 and caspase-3 in the spleen in comparison with results seen in the HFD-C group. Our data suggest that vitamin D supplementation holds promise as an adjunct treatment to alleviate the dysfunction of the spleen and immune system commonly seen in HFD-induced obesity.