Background: Chronic physical stress has many effects on the nervous system and can cause structural changes in different parts of the brain and hemomodulatory, including hormonal. Current pharmacotherapeutic treatments have limited efficacy and are associated with many deleterious side effects. Aim: The aim of this research is to determine how Apis dorsata forest honey administration affects follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels in rats who are subjected to forced swim tests as a model of chronic physical stress placed in a container filled with water from which it cannot escape. Methods: This was an experimental laboratory study with 32 rats divided into four treatment groups: control (C), Treatment 1 (T1) with a forced swim test + honey (2 g/rat/day), Treatment 2 (T2) with a forced swim test + honey (4 g/rat/day), and Treatment 3 (T3) with a forced swim test + honey (6 g/rat/day). All treatments were administered for 14 days. Then, blood was taken for FSH and LH serum tests, and a one-way ANOVA and Duncan test were used to statistically test the data analysis. Results: The results of this study indicate that the administration of forest honey had no significant effect (p > 0.05) on the FSH parameter, but there was a significant decrease in LH levels in the T2 and T3 groups (p < 0.05). Conclusion: It can be concluded that giving forest honey to rats who were subjected to a 14-day forced swim test had no effect on FSH and LH levels. In rats given a forced swim test as a model of chronic stress, administration at doses of 4 and 6 g/rat/day reduced LH serum levels. Thus, giving forest honey could maintain reproductive health in rat that experience chronic stress.
Follicle Stimulating Hormone , Honey , Rats , Bees , Animals , Luteinizing Hormone
Objectives: This study proves the protective effect of Apis dorsata honey against chronic monosodium glutamate (MSG)-induced testicular toxicity on the Leydig cell necrosis count and malondialdehyde (MDA) serum level in Mus musculus mice. Materials and Methods: In this study, 25 male mice were used and grouped into two large groups: The control group consisting of negative control (C-) and positive control (C+). C+ group was fed with 4 mg/g body weight (gBW) of MSG followed by distilled water. The treatment group consisted treatment 1, treatment 2, and treatment 3 groups with A. dorsata honey dosage 53.82 mg/20 g, 107.64 mg/20 g, 161.46 mg/20 g per os (p.o.), respectively, followed by MSG 4 mg/g BW of MSG p.o. For the difference analysis between the group used the one-way ANOVA test and Duncan test. Results: The result of this study showed that there was a significant difference between the treatment group and control group (p<0.05) in the Leydig cell necrosis count and MDA levels. The highest Leydig cell necrosis count and MDA level were found in C+ with values 13.20 ± 2.05 cell and 37.08 ± 9.17 µmol/L compared to C-, while in the treatment group, T3 showed the lowest Leydig cell necrosis value and MDA level 4.64 ± 0.55 cell and 14.22 ± 2.01 µmol/L compared to the C+ group. Conclusion: It can be concluded that A. dorsata honey could reduce the Leydig cell necrosis number and MDA level of mice (Mus musculus) exposed to MSG.
Background and purpose: This study aimed to determine the potency of kebar grass ethanol extract to overcome an increase in cerebellar neuronal cell necrosis, which has an impact on decreasing motor reflex function and spatial memory of mice from lactating mothers exposed to carbofuran. Experimental approach: Forty lactating mice were divided into four groups, 10 each; including control, T1 (carbofuran 0.0125 mg/day), T2 (vitamin C 5 mg + carbofuran 0.0125 mg/day), T3 (kebar grass extract 3.375 mg + carbofuran 0.0125 mg/day). The mice were orally administered with carbofuran, vitamin C, and kebar grass extract on days 0 to 14 postnatal. On the 15th day, brains of the mice were necropsied to measure the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH), H&E staining; motor reflex tests were performed on 10-day-old mice, and the mice aged 30 days were tested on their swimming and spatial memory. Findings / Results: Carbofuran caused an increase in MDA, GSH, neuronal cell necrosis, surface righting reflex, a decrease in SOD, swimming ability, and spatial memory. Kebar grass extract and vitamin C administration decreased MDA, GSH, neuron necrosis, surface righting reflex, and increased SOD, swimming ability, and spatial memory. Conclusion and implications: Exposing to carbofuran in lactating mice caused brain oxidative stress, impaired motor reflexes, and spatial memory in mice offspring. Kebar grass extract and vitamin C administration prevented brain oxidative stress and inhibited disorders in motor reflexes, and spatial memory in mice offspring. Kebar grass extract administration was more effective than vitamin C.
INTRODUCTION: The aim of the study was to describe the process of neuron death in the cerebral cortex caused by embryonic carbofuran exposure. MATERIAL AND METHODS: 81 mouse foetuses from 27 breeding mice were used in the study. Carbofuran was administered by gavage from the 6th to the 15th day of gestation to two groups: one at 0.0208 and the other at 0.0417 mg/kg b.w. On the 17th day, the mice were sacrificed and the foetuses were taken to measure the ROS (malondialdehyde/MDA and superoxide dismutase/SOD) activity in brain tissue, the number of apoptotic embryonic cerebral cortex neurons using a TUNEL assay, and necrotic cells using HE staining. Examination of p53 and caspase 3 expression was done by immunohistochemistry. Data were analysed using analysis of variance (ANOVA) and Duncan's test. RESULTS: Increased activity of cerebral ROS characterised by significant elevation of the MDA level (P < 0.05), decreased SOD (P < 0.01), increased p53 and caspase 3 expression, and cerebral cortical neuron death either by necrosis or apoptosis (P < 0.05) were found. At the low dose carbofuran increased expression of p53, caspase 3, and apoptosis. At the high dose it increased levels of MDA and necrosis. CONCLUSION: Increased expression of p53 and caspase 3 and apoptosis indicated that carbofuran may cause apoptosis through the intrinsic pathway. The increased apoptosis grants an opportunity to prevent and treat the effect of ROS due to gestational carbofuran exposure.
