BackgroundFerula assa foetida commonly consumed as a healthy beverage has been demonstrated to have various biological activities, including antioxidation, anti-obesity and anti-cancer.ObjectiveOur study aims to investigate the antitumor effect of asafoetida in vivo using mouse mammary carcinoma 4T1 cells.Materials and methodsIn the study, female BALB/c mice were divided into two groups (n = 6), which were control (untreated) and other group of mice with breast cancer treated with 100 mg/kg of asafoetida, respectively, by oral gavage. All mice were injected into the mammary fat pad with 4T1 cells (1 × 105 4T1 cells/0.1 ml of phosphate buffer solution). Asafoetida was administered on day 15 after the tumor had developed for 3 weeks. At end of experiment, tumor weight, tumor volume and tumor burden were measured and lung, liver, kidney and tumor were harvested and sections were prepared for histopathological analysis. Lipoxygenase inhibitory and antioxidant activity of asafoetida was also determined.ResultsOur results showed that treatment with asafoetida was effective in decreasing the tumor weight and tumor volume in treated mice. Body weight significantly increased in female BALB/c mice against control. Apart from the antitumor effect, asafoetida decreased lung, liver and kidney metastasis and also increased areas of necrosis in the tumor tissue respectively.ConclusionsThe present study demonstrated that asafoetida has potent antitumor and antimetastasis effects on breast cancer and is a potential source of natural antitumor products.
Introduction:Acrylamide (ACR) consumption is increasing all over the world. There are some evidence on the literature about its neurotoxic effect on mature animals, but the effects of ACR on postnatal development have been less studied. The purpose of this study was to evaluate the effects of ACR on development of cortical layer, white matter, and number of Purkinje cells of the cerebellum in rat newborns.Methods:This study was carried out on 20 female Wistar rats (average weight: 180 g, aged: two months). The rats were divided into four groups. Pregnant rats were orally fed with ACR 10 mg/kg and vitamin C 200 mg/kg. In this study, 6 infants of each group (weighting 32–35 g) were randomly selected at day 21 after birth and placed under deep anesthesia and transcardial perfusion. Their cerebellums were fixed and histopathological changes were evaluated with Hematoxylin and Eosin (H&E) staining and cresyl violet method. The volume of cerebellar cortical layers and number of Purkinje cells were investigated by Cavalieri’s principle and physical dissector methods. The obtained data were analyzed by 1-way ANOVA and LSD test using SPSS. P<0.05 considered as statistically significant.Results:The results showed that newborns of ACR-treated female rats have decreased cerebellar weight (P≤0.05) and lower than average number of Purkinje cells (P≤0.001). ACR also decreased the volume of granular and molecular layer and increased the volume of white matter. While the results showed decreased in white matter volume in vitamin C group (P≤0.001).Conclusion:ACR induces structural changes in the development of the cerebellar cortical layers in rat newborns, but these changes may be prevented by vitamin C as an antioxidant.
BackgroundThe objective of the study was to investigate the protective effects of aqueous extract of Plantago ovata seed (AEPOS) on peptic ulcer induced by indomethacin (IND) in rats.MethodsRats (250-300 g) were divided into three groups (5 rats in each group). Gastric ulcer was induced by a single oral gavage of 48 mg/kg IND. The first group received only 5% sodium bicarbonate orally (5 ml/kg) whereas the control (IND) group received only single oral dose of 48 mg/kg IND. The third group was pretreated with an extract (100 mg/kg) for 4 days. At the end of the 4th day, rats were kept fasted for 24 h before administration of IND 48 mg/kg. The rats were sacrificed 4 h after oral administration of IND and their stomach and liver were fixed in formalin (10%) and sections of 5 mm in diameter were prepared. Histological and morphological characteristics of stomach and liver were assessed using hematoxylin and eosin (H&E) staining.ResultsAEPOS (100 mg/kg) showed a significant (p < 0.05) reduction in microscopic and macroscopic ulcer index as compared to the IND group. Histological analysis indicated that AEPOS has hepatoprotective effect and can prevent mucosa damage in stomach.ConclusionResults revealed that AEPOS has anti-ulcer and hepatoprotective effects.
Sulfur Dioxide (SO 2 ) is a toxic gas with harmful effects on various organs but recent studies, have con rmed the protective effect of SO 2 on ischemic heart disease, atherosclerosis, and lung infections.The present study was designed to investigate the effect of endogenous SO 2 on depression. Chronic Unpredictable Mild Stress (CUMS) model was performed to cause depression. Depression-Like Behaviors in animals were determined using open-eld test, forced swimming test and sucrose consumption. Animal spatial learning and memory was assessed using the Morris water maze. The oxidative status of the hippocampus and serum corticosterone level assessed. A reduction in the tendency to consume sucrose, mobility, and curiosity, as well as learning and memory disorders were observed in CUMS animals. Depressed animals treated with SO 2 showed a signi cant improvement in behavioral and cognitive functions. SO 2 also reduced neuronal damage and lipid peroxidation of the hippocampus and serum corticosterone level in the CUMS group. Various evidences supports a mutual relationship between in ammation and depression, also growing studies shows the role of oxidative stress in the pathogenesis of mood-related disorders such as depression. In this study, increased hippocampal malondialdehyde (MDA) and serum corticosterone levels can be reasons for the existence of oxidative stress and possible activation of in ammatory processes. SO 2 donors reduced MDA and corticosterone levels in depressed animals. According to these results, SO 2 may have been able to reduce tissue damage and eventually behavioral disorders caused by depression by reducing oxidative stress and in ammation.
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