narges haddadzadeh niri

High-cholesterol diet and ensuing oxidative stress causes development of various neurologic disorders. Considering anti-inflammatory and antioxidant properties of the anise (Pimpinella anisum) plant, the effect of its hydroalcoholic extract on hippocampal oxidative stress and cholinesterase activity was assessed in rats under high-cholesterol diet. In this experimental study, rats were divided into control, extract-treated control, high cholesterol diet, and extract-treated high cholesterol diet. After 8 weeks, treated groups also received extract at a dose of 250 mg/kg (i.p.) for 3 weeks and high-cholesterol diet was given till the end of the study. Then, after preparing hippocampal homogenate, butyrylcholinesterase (BChE) activity and oxidative stress factors including reactive oxygen species (ROS), glutathione (GSH), and catalase activity were determined. One-way ANOVA and Tukey's post-hoc tests were used for statistical analysis of data. High cholesterol diet significantly increased hippocampal BChE activity and ROS level and significantly decreased GSH and catalase activity. Conversely, extract treatment of group under high-cholesterol diet caused significant decrease of ROS and BChE activity and significant increase of GSH and with no significant effect on catalase activity. Consumption of anise hydroalcoholic extract under high-cholesterol diet reduces hippocampal oxidative stress and cholinesterase activity and this may lower associated neurological complications.

High-cholesterol diet and ensuing inflammation cause liver disorders and damage. Considering the anti-inflammatory and antioxidant properties of the anise plant, the effect of its hydroalcoholic extract on the activity of liver enzymes was assessed in rats under a high-cholesterol diet. In this experimental study, rats were divided into control, extract-treated control, high cholesterol diet, and extract-treated high cholesterol diet. After 8 weeks, that the control groups received normal food and the high-fat groups received high-cholesterol food, treated groups also received extract at a dose of 250 mg/kg (i.p.) for 3 weeks and consumption of high-cholesterol diet continued till the end of study. At the end, after obtaining blood samples, serum activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) enzymes was measured. One-way ANOVA and Tukey's post-hoc tests were used for the statistical analysis of data. High-cholesterol diet significantly increased serum activity of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase. Conversely, extract treatment of the group under a high-cholesterol diet caused a significant decrease in the activity of these enzymes. Consumption of anise hydroalcoholic extract under a high-cholesterol diet reduces the serum level of liver enzymes and this may lower the incidence of liver diseases.

Temporal lobe epilepsy is characterized by the degeneration of hippocampal neurons and the sprouting of mossy fibers in the dentate area. This study aimed to investigate the impact of the hydroalcoholic extract of Rosa damascene on hippocampal tissue changes induced by kainic acid-induced epilepsy in rats.

In this experimental study, 28 male Wistar rats weighing between 185-225 grams were used. The animals were divided into four groups: sham group, sham treated with hydroalcoholic extract, epilepsy (kainic acid), and epilepsy pretreated with hydroalcoholic extract. Kainic acid was used for intra-hippocampal and unilateral injection to induce epilepsy in the animals at 0.8 micrograms per rat. The rats were given 500 mg/kg of the extract intraperitoneally daily for one week before surgery. Five weeks after surgery, thionin and Tim staining methods were performed on the hippocampal slices.

Kainic acid-induced epilepsy resulted in convulsive behavior, and pretreatment with the hydroalcoholic extract significantly reduced the intensity of convulsive attacks (P<0.05). The density of neurons in the CA3 area of the hippocampus in the kainic acid group showed a significant decrease compared to the sham group (P<0.05), while pretreatment with the extract caused a significant increase in the number of neurons in this area compared to the kainic acid group. Additionally, a significant increase in the intensity of mossy fiber sprouting was observed in epileptic rats compared to the sham group, and pretreatment with the extract significantly decreased its intensity (P<0.05).

The pre-treatment with the hydroalcoholic extract of Rosa damascena decreased convulsive behavior, protected hippocampal CA3 neurons and reduced the intensity of sprouting in the hippocampal dentate region in the experimental model of temporal lobe epilepsy induced by kainic acid.

Acrylamide is a neurotoxic agent that increases oxidative stress by creating an imbalance between the production and removal of free radicals, which in turn contributes to the pathogenesis of some neurodegenerative disorders. Thymoquinone extracted from Nigella satvia has prominent antioxidant effects. The objective of this study was to evaluate the effects of thymoquinone on hippocampal oxidative stress and neuronal density following acrylamide administration in male rats.

In this experimental study, 28 male Wistar rats aged 10-12 weeks and weighing 180-200 g were randomly divided into 4 groups of 7 rats: control, acrylamide, acrylamide + thymoquinone treatment (1 mg/kg), and acrylamide + thymoquinone treatment (5 mg/kg). For induction of brain injury, 50 mg/kg of acrylamide was injected intraperitoneally. Two days after the acrylamide injection, the rats were sacrificed, and malondialdehyde (MDA), glutathione (GSH), and catalase levels were measured in hippocampal homogenate. Evaluation of neuronal density in hippocampal CA1 region was also performed by Nissl staining.

Acrylamide injection significantly increased MDA level and reduced GSH content and catalase activity in comparison with the control group (P<0.05). Administration of 5 mg/kg thymoquinone significantly reduced MDA level (P<0.05) but improved GSH and catalase activity in comparison with the acrylamide group (P<0.05). In addition, neuron density of hippocampal CA1 region did not differ significantly between the groups.

Thymoquinone can attenuate oxidative stress markers in a dose-dependent manner.

Acute liver injury is a fatal syndrome that causes rapid loss of liver function. Crocin is the active ingredient of saffron with antioxidant, protective and anti-apoptotic properties. In this study, the protective effect of crocin was evaluated on the liver dysfunction in male laboratory mice.

In this experimental study, 28 male mice (20-24 g) were divided into control, liver damage, and two groups treated with crocin at doses of 50 or 200 mg/kg. liver damage was caused by the injection of lipopolysaccharide/D-galactosamine with doses of 50 microg/kg and 400 mg/kg, respectively. Crocin dissolved in distilled water was fed by gavage at 50 or 200 mg/kg, starting 3 days before and up to 1 hour before injury induction. 24 hours after injury induction, the mice were anesthetized with a mixture of 120 mg/kg ketamine and 10 mg/kg xylazine, and sacrificed in compliance with ethical rules after taking a blood sample from their hearts. liver markers including MDA, SOD, Cat, MPO, and TNF-α were measured. Data was analyzed with GraphPad Prism 9.3 software using one-way ANOVA and Tukey's post hoc tests with significance level set at p<0.05.

Administration of crocin decreased serum levels of liver markers MDA, MPO, and TNF-α and increased SOD in crocin-treated groups as compared to the LPS/D-Gal group (p<0.05); Cat change was not significant (p>0.05).

Crocin with strong antioxidant activity was able to reduce liver dysfunction by reducing oxidative stress and inflammation.

Long-term exposure to glucocorticosteroids is associated with brain damage through augmenting oxidative stress and apoptotic cell death. Due to the anti-oxidative and anti-apoptotic effects of ferulic acid (FA), its effect on learning, memory, and protection of the hippocampus in dexamethasone (DEX) treated rats were investigated in this study.

This experimental study was conducted on 32 male Wistar rats. Neural injury was induced by injection of 500 µg/kg/day of DEX for 3 weeks. Treatment groups received oral FA (50 mg/kg/day) for 3 weeks. At the end of 3rd week and following evaluation of learning and memory by passive avoidance and novel object discrimination (NOD) tests, some related factors of oxidative stress and apoptosis in hippocampal homogenate were measured and number of neurons in hippocampal CA1 area was also counted.

Step-through latency and discrimination index were significantly higher in FA-treated DEX group than DEX group. FA-treatment of DEX group was associated with lower levels of MDA, caspase 1, and caspase 3 but higher activity of superoxide dismutase (SOD). Meanwhile, CA1 neuronal density was significantly higher in FA-treated DEX group.

Taking ferulic acid simultaneously with long-term administration of dexamethasone prevents the occurrence of learning and memory disorders and hippocampus damage, and part of its beneficial effect is done through reducing oxidative stress and apoptosis.

The liver is the largest gland in the body with multiple functions. Methotrexate causes acute and chronic liver damage. In this study, the effects of diosgenin were investigated as a steroidal sapogenin on mitochondrial membrane potential (MMP) and neutrophil infiltration activity in a methotrexate-induced liver injury model in male rats.

40 rats in 5 groups; control, control treated with diosgenin 50 mg/kg, methotrexate at a dose of 20 mg/kg (i.p) and two groups treated with diosgenin at doses 10, 50 mg/kg (gavage) were divided. The rats were anesthetized and the liver tissue was isolated after killing. After tissue homogeneity, neutrophil infiltration activity and mitochondrial membrane potential were measured. For statistical analysis, one-way ANOVA and Tukey post-test were used, and the significance level was p <0.05.

The potential of the mitochondrial membrane in the methotrexate group treated with diosgenin 10 mg/kg was significantly reduced compared to the control group and in the group treated with diosgenin 50 mg/kg was significantly increased compared to methotrexate. On the other hand, myeloperoxidase increased significantly in the methotrexate group and treated with diosgenin 10 mg/kg compared to the control group and decreased significantly in the group treated with diosgenin 50 mg/kg compared to the methotrexate group.

Diosgenin at a dose of 50 mg/kg in the methotrexate-induced liver injury model was able to improve mitochondrial health and reduced neutrophil infiltration.