فهرست مطالب safoura raoufi

Diabetes mellitus is associated with memory impairment. Ellagic acid (EA) is a natural polyphenol with anti-diabetic and neuroprotective effects. The aim of the present study was to investigate the protective effect of ellagic acid on diabetes induced memory impairment and to evaluate the role of its antioxidant effect. Male Wistar rats were randomly divided into four groups (n=8): control, diabetic, diabetic receiving 25 mg/kg of EA, and diabetic receiving 50 mg/kg of EA. Diabetes was induced by a single intraperitoneal injection of 60 mg/kg of streptozotocin (STZ). After receiving EA (once a day) by oral gavage for four weeks, passive avoidance learning (PAL) test was used to evaluate memory. Finally, oxidative stress related factors including malondialdehyde (MDA) and total antioxidant capacity (TAC) were evaluated in the hippocampal tissue separated from the animal brains under deep anesthesia. Diabetic animals showed marked reductions in step-through latency (STLr) and elevation in time spent in the dark compartment (TDC)  in the retention trial and elevation of MDA level and diminution of TAC compared to controls significantly. Treatment of diabetic rats with EA markedly increased STLr, decreased TDC and enhanced TAC (by both EA doses) and reduced MDA (at a dose of 50 mg/kg of EA). The results displayed learning and memory improving effect of EA in diabetic rats via attenuating oxidative stress.

Hyperalgesia is among the current complications of diabetes mellitus; oxidative stress and inflammation were influential in its development. As an herbal component, Ellagic Acid (EA) has some biological activities, including antioxidant and anti-inflammatory effects. This study was designed to evaluate the possible beneficial effect of EA on hypernociception in Streptozotocin (STZ)-induced hyperglycemic rats.

Forty-eight male Wistar rats were divided into the control (receiving vehicle), hyperglycemic, EA (25 mg/kg)-treated control, EA (50 mg/kg)-treated control, EA (25 mg/kg)-treated hyperglycemic, and EA (50 mg/kg)-treated hyperglycemic groups. Hyperglycemia was induced by a single Intraperitoneal (IP) injection of STZ (60 mg/Kg). EA was administered daily by oral gavage for four weeks. The nociceptive response was assessed using Tail-Flick (TF) and Hot-Plate (HP) tests. Also, oxidative stress markers, including Malondialdehyde (MDA), Total Oxidant Status (TOS), and Total Antioxidant Capacity (TAC) in the serum, were evaluated.

Hyperglycemic animals were found with significant changes, including a reduction in TF and HP latencies, an elevation in serum MDA level and TOS, and a decrease in serum TAC compared with controls. The treatment of hyperglycemic rats with EA facilitated the reduction of TF latency at the dose of 25 mg/kg and HP latency at 50 mg/kg. Furthermore, EA significantly increased TAC and decreased MDA level at a 50 mg/kg dose and reduced TOS at both doses in the serum of hyperglycemic animals. No significant alterations were found in the parameters studied in EA-treated normal rats.

These results displayed the antinociceptive effect of EA in hyperglycemic rats via attenuating oxidative stress. Therefore, EA appears to be a promising agent for managing. Hyperglycemic hypernociception.

Today, drug addiction is an important healthcare issue. Any helps to drug withdrawal may decrease its prevalence in the society. Ascorbic acid is a component, which can affect neurotransmitter systems as a regulator along with its cofactor role. Noradrenergic and dopaminergic systems are two important neurotransmitter systems in the opiate withdrawal syndrome. It seems that ascorbic acid can decrease the symptoms of opiate withdrawal through regulating the related systems. In this regard, the current study aimed to evaluate the effect of ascorbic acid on the symptoms of morphine withdrawal in Syrian mice.

Male Syrian mice in eight experimental groups received incremental doses of morphine as 10, 20, 30 and 40mg/kg within the first, second, third, and fourth days of the experiment, respectively, through intraperitoneal injection, twice a day, and the control group received and equal amount of saline. On the fifth day, six groups of morphine addicts received ascorbic acid with six doses of 10, 50, 100, 200, 400 and 800mg/kg through intraperitoneal injection. Then, naloxone 2mg/kg was injected to all groups including morphine alone and morphine with acute does of ascorbic acid. Then, withdrawal symptoms were evaluated for 30 minutes.

Administration of an acute dose of ascorbic acid reduced dose dependent withdrawal symptoms in such a way that 10, 50, and 100mg/kg doses of ascorbic acid reduced “writhing” symptom, 200mg/kg reduced “jumping” symptom, and 400 and 800mg/kg reduced “climbing, jumping, and standing” symptoms.

It seems that ascorbic acid administration can improve the symptoms of opiate withdrawal syndrome. More studies on human population can also indicate the therapeutic effect of ascorbic acid on drug withdrawal.

Oxidative stress induced by proinflammatory cytokines such as IL-1β plays a major role in β-cell destruction in diabetes type 1. Salvianolic acid B (Sal B) is a polyphenolic compound with antioxidant and protective effects. Thus, objective of this study was to assess the protection exerted by Sal B on isolated rat islets exposed to IL-1β and to investigate an underlying mechanism in vitro.
Isolation of pancreatic islets was done by using the collagenase digestion method. Isolated rat islets were divided into 6 groups including: 1. control, 2. interleukin-1β treated, 3 and 4. interleukin-1β treated Sal B, 5 and 6. interleukin-1β treated Sal B PKB and PI3K inhibitors. Interleukin-1β (1 U/ml) was used to induce cytotoxicity after pretreatment with two doses of Sal B (50 μM and 100 μM) and application of each inhibitors was before Sal B.
IL-1β significantly decreased insulin secretion from isolated islets. Pretreatment with Sal B ameliorated the effect of IL-1β on glucose stimulated insulin secretion in a concentration dependent manner. Inhibitors of PKB and PI3K both abolished these improving effect of Sal B.
Sal B that has antioxidant, anti inflammatory and anti apoptotic properties, provided resistance to pancreatic β-cell dysfunction from cytokine in part via PI3K/Akt pathway. The findings represent that it is a promising agent for prevention of β-cell dysfunction in type 1 diabetes.

A huge amount of investigational evidence support a role for oxidative stress as an intermediary of nerve cell dysfunction in Parkinson’s disease (PD). Polyphenols such as carvacrol have been indicated to prevent neuronal deterioration caused by increased oxidative load, thus, this study evaluated whether carvacrol administration would attenuate behavioral abnormalities in an animal model of PD. In this study, unilateral intrastriatal 6-hydroxydopamine injected rats were daily pretreated with carvacrol (10 mg/kg) started three days before the surgery. Apomorphine-induced rotations and level of stress oxidative markers in the midbrain were assessed after 2 weeks. Carvacrol administration lessened the rotation number in lesioned rats. Also, carvacrol decreased the 6-OHDA-induced malondialdehyde and nitrite level and intensified the antioxidant enzyme catalase, indicative of a protective effect against lipid peroxidation and free radicals synthesis. In summary, carvacrol shows a protective effect against 6-OHDA neurotoxicity, partly through attenuating oxidative stress.