Histopathological and Biochemical Assessment of Neuroprotective Effects of Sodium Valproate and Lutein on the Pilocarpine Albino Rat Model of Epilepsy.

Epilepsy is one of the most frequent neurological disorders characterized by an enduring predisposition to generate epileptic seizures. Oxidative stress is believed to directly participate in the pathways of neurodegenerations leading to epilepsy. Approximately, one-third of the epileptic patients who suffer from seizures do not receive effective medical treatment. Sodium valproate (SVP) is a commonly used antiepileptic drug (AED); however, it has toxic effects. Lutein (L), a carotenoid, has potent antioxidant and anti-inflammatory properties. The aim of this study was to determine the neuroprotective effect of sodium valproate (SVP) and lutein (L) in a rat model of pilocarpine- (PLC-) induced epilepsy. To achieve this aim, fifty rats were randomly divided into five groups. Group I: control, group II: received PLC (400 mg/kg intraperitoneally), group III: received PLC + SVP (500 mg/kg orally), group IV: received PLC + SVP + L (100 mg/kg orally), and group V: received (PLC + L). Racine Scale (RC) and latency period to onset seizure were calculated. After eight weeks, the hippocampus rotarod performance and histological investigations were performed. Oxidative stress was investigated in hippocampal homogenates. Results revealed that SVP and L, given alone or in combination, reduced the RC significantly, a significant delay in latency to PLC-kindling onset, and improved rotarod performance of rats compared with the PLC group. Moreover, L was associated with a reduction of oxidative stress in hippocampal homogenate, a significant decrease in serum tumor necrosis factor-alpha (TNF-α) level, and inhibition of cerebral injury and displayed antiepileptic properties in the PLC-induced epileptic rat model. Data obtained from the current research elucidated the prominent neuroprotective, antioxidant, and anti-inflammatory activities of lutein in this model. In conclusion, lutein cotreatment with AEDs is likely to be a promising strategy to improve treatment efficacy in patients suffering from epilepsy.

The Neuroprotective Effect of Carvedilol on Diabetic Neuropathy: An In Vitro Study.

Diabetic neuropathy serves as a major complication for diabetic patients across the world. The use of effective treatment is integral for reducing the health complications for diabetic patients. This study has evaluated the carvedilol potential neuroprotective effect on diabetic neuropathy. An in vitro model of diabetic neuropathy was used, including dorsal root ganglia (DRG) that were cultured from male adult mice C57BL. These were incubated for about twenty-four hours in high glucose (HG) media (45 mM). Some cells were incubated with carvedilol (10 µM). Neuronal viability, neuronal morphology, and activating transcription factor 3 (AFT3) were measured. The cell viability was decreased, along with neuronal length, soma area, and soma perimeter with HG media. Also, there was an overexpression of ATF3, which is a neuronal stress response marker. The pretreatment with carvedilol increased the viability of DRG as compared to HG-treated cells. Also, it significantly protected the DRG from HG-induced morphology changes. Though it shows a decrease in AFT3 expression, the statistical results were insignificant. The current study demonstrates the neuroprotective effect of carvedilol against HG-induced DN using an in vitro model. This could be through carvedilol antioxidant effects.

Ghrelin gastric tissue expression in patients with morbid obesity and type 2 diabetes submitted to laparoscopic sleeve gastrectomy: immunohistochemical and biochemical study.

INTRODUCTION: Obesity and type 2 diabetes mellitus (T2DM) are leading causes of morbidity and mortality worldwide. Ghrelin is implicated in the pathophysiology of both disease states. Laparoscopic sleeve gastrectomy is an emerging safe therapeutic technique for patients with morbid obesity. Since the removal of ghrelin-secreting cells by sleeve gastrectomy may be associated with diminished hunger sensation the aim of the study was to: (i) compare body weight and body mass index (BMI) in both obese non-diabetic and obese diabetic patient groups, (ii) determine the ghrelin expression in the resected gastric tissue in both groups, (iii) evaluate relationships between ghrelin cell expression and pre- and post-operative serum ghrelin concentration and glucose levels, and (iv) assess the influence of sleeve gastrectomy on serum glycaemic parameters in this patient population. MATERIAL AND METHODS: Twenty morbidly obese female patients from Saudi Arabia, of whom ten suffered from T2DM participated in the study. All subjects underwent laparoscopic sleeve gastrectomy. The removed fundus, body and antrum were biopsied and underwent immunohistochemical staining to detect ghrelin cell expression. Serum samples were assayed for ghrelin concentration and indicators of glycaemic status at the baseline and three months after sleeve gastrectomy. RESULTS: BMI (p < 0.05) and body weight (p < 0.001) were significantly lower in non-diabetic obese patients compared with diabetic patients before and 3 months after the surgery. Also, pre-operative serum ghrelin level was higher in non-diabetic patients compared with diabetic patients group, and postoperative plasma ghrelin level was reduced in diabetic patients (p < 0.001) compared with non-diabetic patients. Gastric fundic mucosa of the diabetic patients exhibited lower number of ghrelin-positive cells (p < 0.05) compared with non-diabetic patients. There were significant negative correlations between pre- and post-operative ghrelin serum level and blood glucose (r = -0.736, p = 0.0002 and r = -0.656, p = 0.0007, respectively) in all patient populations. CONCLUSIONS: The results of this study suggest that the diabetic status of obese female patients may affect the incidence of ghrelin cells in three major stomach's regions and this novel observation warrants further studies.