Assessment of Cinnamaldehyde's Potency on Heat Stress-induced Testicular Impairments in Wistar Rats.

Background: Male sterility results from high testicular temperatures, which affect mammalian spermatogenesis. High testicular temperatures affect sperm motility, morphology and fertility according to their magnitude and duration. Aim: The aim of the current study is to examine the effects of heat-induced oxidative stress and cinnamaldehyde on Wistar rat testicular structure and function. Settings and Design: The rats used in this experiment were Wistar albino rats. Materials and Methods: This research has six animals per group. Male Wistar albino rats of 2.5-3 months old and 275-300 g. (I) control, (II) heat stress (HS) in a closed chamber at 41°C for 14 days and (III) HS with cinnamaldehyde (CA) 50 mg/kg body weight for 14 days. (IV) CA alone. After the study, the animals were euthanised, and test samples were taken for sperm count, morphology, haematoxylin and eosin stain for normal cellular morphology, antioxidants and DNA integrity assessments. Statistical Analysis Used: The data were analysed statistically using one- and two-way ANOVA tests for comparisons between groups. Results: The stress group had significantly lower sperm counts and poor sperm morphology. The stress group's antioxidant capacity is much lower than that of the control group. Animals under stress have fragmented DNA. Treatment with cinnamaldehyde increased overall antioxidant capacity and seminal parameters, and rats behaved most like controls. Conclusion: CA restores malondialdehyde levels, total antioxidant capacity, sperm characteristics and mitigates testicular damage in rats exposed to experimental HS.

Aspartame Causes Developmental Defects and Teratogenicity in Zebra Fish Embryo: Role of Impaired SIRT1/FOXO3a Axis in Neuron Cells.

Aspartame, a widely used artificial sweetener, is present in many food products and beverages worldwide. It has been linked to potential neurotoxicity and developmental defects. However, its teratogenic effect on embryonic development and the underlying potential mechanisms need to be elucidated. We investigated the concentration- and time-dependent effects of aspartame on zebrafish development and teratogenicity. We focused on the role of sirtuin 1 (SIRT1) and Forkhead-box transcription factor (FOXO), two proteins that play key roles in neurodevelopment. It was found that aspartame exposure reduced the formation of larvae and the development of cartilage in zebrafish. It also delayed post-fertilization development by altering the head length and locomotor behavior of zebrafish. RNA-sequencing-based DEG analysis showed that SIRT1 and FOXO3a are involved in neurodevelopment. In silico and in vitro analyses showed that aspartame could target and reduce the expression of SIRT1 and FOXO3a proteins in neuron cells. Additionally, aspartame triggered the reduction of autophagy flux by inhibiting the nuclear translocation of SIRT1 in neuronal cells. The findings suggest that aspartame can cause developmental defects and teratogenicity in zebrafish embryos and reduce autophagy by impairing the SIRT1/FOXO3a axis in neuron cells.

Noise and brain.

Noise has become inexorable stress due to the increase in urbanization, automobile usage, Noise based occupation, and lifestyle modifications such as recreation in day to day life of an individual. Noise not only affects the auditory system but can also debilitate other non-auditory systems as evidenced in animal and human models. Various studies have reported that noise has the potential to tarnish the Central Nervous System in heterogeneous ways. This article reviews the researches on Noise and Brain with the spotlight on the effect of noise on health that includes a) noise-induced impaired cognition on neurobehaviour, b) brain areas which are predominantly affected by the noise-induced oxidative stress, c) alteration of the neurotransmitter level in various brain regions, d) alteration of the molecular mechanism induced by noise stress on brain cellular level, e) Noise-induced deterioration of the morphological structures of brain and f) epigenetic modification by noise on brain.

Effect of Yoga Intervention on Short-Term Heart Rate Variability in Children with Autism Spectrum Disorder.

BACKGROUND: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairment in social interactions, communication, restricted, and repetitive behaviors. Evidence-based treatment options for ASD are limited. Yoga is practiced by over 20 million people worldwide, and multiple studies have investigated yoga as a possible effective intervention for children with ASD. AIM: The aim of this study is to investigate the effect of yoga intervention on short-term heart rate variability (HRV) in children with ASD. METHODOLOGY: In this study, 50 children (38 boys and 12 girls) with ASD were recruited from Swabhimaan Trust, Palavakkam, Chennai. They were randomly grouped into ASD with yoga intervention group (n = 25) and ASD without yoga intervention group (n = 25) by simple lottery method. Yoga group children underwent yoga training for 3 months, and the control group did not receive any such training. For short-term HRV, 15 min electrocardiogram recording in sitting posture was recorded in lead II using a simple analog amplifier. RESULTS: In HRV, time domain parameters such as mean RR interval (0.72 [0.74] to 0.94 [0.92]), standard deviation of the NN intervals (52.04 [54.23] to 74.48 [72.80]), and root of the mean squared differences of successive NN interval (32.60 [34.40] to 40.83 [42.90]) significantly increased in ASD children after yoga intervention. In frequency-domain parameters, high frequency (HF) in n. u (48.08 [47.24] to 58.37 [59.22]) shows a significant increase and low frequency (LF) in n. u (52.4 [51.82] to 40.51 [40.12]), and LF/HF ratio (1.29 [1.31] to 0.78 [0.79]) shows a significant decrease in ASD with yoga intervention group children after 3 months of yoga training. CONCLUSION: Yoga interventions have been successful in bringing parasympathetic dominance in ASD children, and the greater advantage is being a noninvasive way of intervention to support children with ASD and help them to achieve physiological as well as psychological balance.

Oxidative stress evoked damages leading to attenuated memory and inhibition of NMDAR-CaMKII-ERK/CREB signalling on consumption of aspartame in rat model.

Many controversial reports are available on the use of aspartame as it releases methanol as one of its metabolite during metabolism. The present study proposes to investigate whether long term (90 days) aspartame (40 mg/kg b.wt) administration could induce oxidative stress and alter the memory in Wistar strain male albino rats. To mimic the human methanol metabolism, methotrexate (MTX)-treated rats were included as a model to study the effects of aspartame. Wistar strain albino rats were administered with aspartame (40 mg/kg b.wt) orally and studied along with controls and MTX-treated controls. Aspartame interfered in the body weight and corticosterone levels in the rats. A marked increase in the mRNA and protein expression of neuronal nitric oxide synthase (nNOS) and induced nitric oxide synthase (iNOS) which resulted in the increased nitric oxide radical's level indicating that aspartame is a stressor. These reactive nitrogen species could be responsible for the altered cell membrane integrity and even cause death of neurons by necrosis or apoptosis. The animals showed a marked decrease in learning, spatial working and spatial recognition memory deficit in the Morris water maze and Y-maze performance task which could have resulted due to reduced hippocampal acetylcholine esterase (AChE) activity. The animal brain homogenate also revealed the decrease in the phosphorylation of NMDAR1-CaMKII-ERK/CREB signalling pathway, which well documents the inhibition of phosphorylation leads to the excitotoxicity of the neurons and memory decline. This effect may be due to methanol which may also activate the NOS levels, microglia and astrocytes, inducing neurodegeneration in brain. Neuronal shrinkage of hippocampal layer due to degeneration of pyramidal cells revealed the abnormal neuronal morphology of pyramidal cell layers in the aspartame treated animals. These findings demonstrate that aspartame metabolites could be a contributing factor for the development of oxidative stress in the brain.

Maternal psychological stress-induced developmental disability, neonatal mortality and stillbirth in the offspring of Wistar albino rats.

BACKGROUND: Stress is an inevitable part of life, and maternal stress during the gestational period has dramatic effects in the early programming of the physiology and behavior of offspring. The developmental period is crucial for the well-being of the offspring. Prenatal stress influences the developmental outcomes of the fetus, in part because the developing brain is particularly vulnerable to stress. The etiology of birth defects of the offspring is reported to be 30-40% genetic and 7-10% multifactorial, with the remaining 50% still unknown and also there is no clear cause for neonatal mortality and still-birth. OBJECTIVE: The present study explores the association of maternal psychological stress on mother and the offspring's incidence of birth defects, stillbirth, and neonatal mortality. STUDY DESIGN: Pregnant animals were restrained to induce psychological stress (3 times per day, 45 minutes per session). Except control group, other animals were exposed to restraint stress during the gestational period: early gestational stress (EGS, stress exposure during 1st day to 10th days of gestational period), late gestational stress (LGS, stress exposure during 11th day to till parturition), and full term gestational stress (FGS, stress exposure to the whole gestational period). The effects of maternal stress on the mother and their offspring were analyzed. RESULTS: Expectant female rats exposed to stress by physical restraint showed decreased body weight gain, food intake, and fecal pellet levels. Specifically, the offspring of female rats subjected to late gestational and full term gestational restraint stress showed more deleterious effects, such as physical impairment (LGS 24.44%, FGS 10%), neonatal mortality (EGS 2.56%, LGS 24.44%, FGS 17.5%), stillbirths (FGS 27.5%), low birth weight (EGS 5.42g, LGS 4.40g, FGS 4.12g), preterm births (EGS 539 Hrs, LGS 514 Hrs, FGS 520.6 Hrs), and delayed eyelid opening (EGS 15.16 Days, LGS 17 Days, FGS 17.67 Days). CONCLUSION: The results of this study reveal that maternal stress may be associated with the offspring's abnormal structural phenotyping, preterm birth, stillbirth and neonatal mortality.

Antioxidant mediated response of Scoparia dulcis in noise-induced redox imbalance and immunohistochemical changes in rat brain.

Noise has been regarded as an environmental/occupational stressor that causes damages to both auditory and non-auditory organs. Prolonged exposure to these mediators of stress has often resulted in detrimental effect, where oxidative/nitrosative stress plays a major role. Hence, it would be appropriate to examine the possible role of free radicals in brain discrete regions and the "antioxidants" mediated response of S. dulcis. Animals were subjected to noise stress for 15 days (100 dB/4 hours/day) and estimation of endogenous free radical and antioxidant activity were carried out on brain discrete regions (the cerebral cortex, cerebellum, brainstem, striatum, hippocampus and hypothalamus). The result showed that exposure to noise could alleviate endogenous free radical generation and altered antioxidant status in brain discrete regions when compared to that of the control groups. This alleviated free radical generation (H2O2 and NO) is well supported by an upregulated protein expression on immunohistochemistry of both iNOS and nNOS in the cerebral cortex on exposure to noise stress. These findings suggest that increased free radical generation and altered anti-oxidative status can cause redox imbalance in the brain discrete regions. However, free radical scavenging activity of the plant was evident as the noise exposed group treated with S. dulcis[200 mg/(kg·b·w)] displayed a therapeutic effect by decreasing the free radical level and regulate the anti-oxidative status to that of control animals. Hence, it can be concluded that the efficacy of S. dulcis could be attributed to its free radical scavenging activity and anti-oxidative property.

Role of Scoparia dulcis linn on noise-induced nitric oxide synthase (NOS) expression and neurotransmitter assessment on motor function in Wistar albino rats.

Noise pollution is one of the most widespread and fast growing environmental and occupational menaces in the modern era. Exposure to noise above 100dB is not adaptable through the brain homeostatic mechanism. Yet, the detrimental effects of noise have often been ignored. Developing reliable animal models to understand the neurobiology of noise stress and advance our research in the field of medicine to impede this growing stressor is needed. In this study experimental animals were divided into four groups, (i) Control and (ii) S. dulcis extract (200mg/kgbw) treated control group. (iii) To mimic the influence of noise, animals in this group were exposed to noise stress (100dB/4h/day) for 15days and finally, (iv) Noise exposed treated with S. dulcis extract (200mg/kgbw) group. Rota-rod and narrow beam performance results showed impaired motor co-ordination in noise exposed group on both 1st and 15th day when compared to controls. This impaired motor function on exposure to noise could be attributed to the altered norepinephrine, dopamine and serotonin levels in both the striatum and cerebellum. Moreover, the motor impaired associated changes could also be attributed to upregulated nNOS and iNOS protein expression in the cerebellum resulting in increased nitric oxide radical production. This increased reactive free radicals species can initiate lipid peroxidation mediated changes in the cerebellar Purkinje cells, which is responsible for initiating inhibitory motor response and ultimately leading to impaired motor co-ordination. Treatment with S. dulcis extract (200mg/kgbw) could control motor impairment and regulate neurotransmitter level as that of control groups when compared to noise exposed group. One key aspect of therapeutic efficacy of the plant could have resulted due to attenuated lipid peroxidation mediated damages on the cerebellar Purkinje cells thereby regulating motor impairment. Thus, targeting the antioxidant and free radicals scavenging properties of the plant could serve as a potential therapeutic to combat this environmental stressor.

Free radical scavenging potential and HPTLC analysis of Indigofera tinctoria linn (Fabaceae).

The objective of this study was to evaluate the free radical scavenging potential and high performance thin layer chromatography (HPTLC) fingerprinting of Indigofera tinctoria (I. tinctoria). Phytochemical analysis was carried out using standard methods, and free radical scavenging activity of the plant was determined using 2,2-diphenyl-1-picrylhydrazy (DPPH), nitric oxide (NO) and superoxide anion ([Formula: see text]) radical scavenging capacities. HPTLC plate was kept in CAMAG TLC Scanner 3 and the Rf values at fingerprint data were recorded by WINCATS software. Aqueous extract of I. tinctoria reliably showed the total phenolics (267.2±2.42 mg/g), flavonoids (75.43±3.36 mg/g) and antioxidants (349.11±8.04 mg/g). The extract was found to have DPPH (52.08%), NO (23.12%) and [Formula: see text] (26.79%) scavenging activities at the concentration of 250 µg/mL and the results were statistically significant compared with ascorbic acid standard (p<0.05). HPTLC results confirmed that the extract contained several potential active components such as phenols, flavonoids, saponins and terpenoids as the slides revealed multi-colored bands of varying intensities. This study confirmed that the plant had multipotential antioxidant and free radicals scavenging activities.