Autism spectrum disorders (ASD) is a group of generalized neurodevelopmental disorders. Its main clinical features are social communication disorder and repetitive stereotyped behavioral interest. The abnormal structure and function of brain network is the basis of social dysfunction and stereotyped performance in patients with autism spectrum disorder. The number of patients diagnosed with ASD has increased year by year, but there is a lack of effective intervention and treatment. Oxytocin has been revealed to effectively improve social cognitive function and significantly improve the social information processing ability, empathy ability and social communication ability of ASD patients. The change of serotonin level also been reported affecting the development of brain and causes ASD-like behavioral abnormalities, such as anxiety, depression like behavior, stereotyped behavior. Present review will focus on the research progress of serotonin and oxytocin in the pathogenesis, brain circuit changes and treatment of autism. Revealing the regulatory effect and neural mechanism of serotonin and oxytocin on patients with ASD is not only conducive to a deeper comprehension of the pathogenesis of ASD, but also has vital clinical significance.

Genus Hypericum (Guttiferae, Hypericoideae) is perennial, belonging to the Hypericaceae family, having 484 species in forms of trees, shrubs, and herbs, distributed in 36 taxonomic sections. No detailed Random Amplified Polymorphic DNA (RAPD) studies were conducted to study Hypericum genetic diversity. Therefore, we collected and analyzed six species from five provinces of Iran regions. Overall, seventy plant specimens were collected. Our aims were 1) to assess genetic diversity among Hypericum species 2) is there a correlation between species genetic and geographical distance? 3) Genetic structure of populations and taxa. We showed significant differences in quantitative morphological characters in plant species. H. dogonbadanicum depicted unbiased expected heterozygosity (UHe) in the range of 0.10. Shannon information was high (0.32) in H. perforaturm. H. dogonbadanicum showed the lowest value, 0.17. The observed number of alleles (Na) ranged from 0.22 to 0.53 in H. dogonbadanicum and H. elongaturn. Gene flow (Nm) was relatively low (0.87) in Hypericum. The Mantel test showed correlation (r = 0.45, p=0.0001) between genetic and geographical distances. We reported high genetic diversity, which clearly shows the Hypericum species can adapt to changing environments since high genetic diversity is linked to species adaptability. Present results highlighted the utility of RAPD markers and morphometry methods to investigate genetic diversity in Hypericum species.

Epidemiological surveys and studies with animal models have established a relationship between maternal stress and affective disorders in their offspring. However, whether maternal depression before pregnancy influences behaviour and related neurobiological mechanisms in the offspring has not been studied. A social defeat stress (SDS) maternal rat model was established using the resident-intruder paradigm with female specific pathogen-free Wistar rats and evaluated with behavioural tests. SDS maternal rats showed a significant reduction in sucrose preference and locomotor and exploratory activities after 4 weeks of stress. In the third week of the experiment, a reduction in body weight gain was observed in SDS animals. Sucrose preference, open field, the elevated-plus maze, light–dark box, object recognition, the Morris water maze, and forced swimming tests were performed using the 2-month-old male offspring of the female SDS rats. Offspring subjected to pre-gestational SDS displayed enhanced anxiety-like behaviours, reduced exploratory behaviours, reduced sucrose preference, and atypical despair behaviours. With regard to cognition, the offspring showed significant impairments in the retention phase of the object recognition test, but no effect was observed in the acquisition phase. These animals also showed impairments in recognition memory, as the discrimination index in the Morris water maze test in this group was significantly lower for both 1 h and 24 h memory retention compared to controls. Corticosterone, adrenocorticotropic hormone, and monoamine neurotransmitters levels were determined using enzyme immunoassays or radioimmunoassays in plasma, hypothalamus, left hippocampus, and left prefrontal cortex samples from the offspring of the SDS rats. These markers of hypothalamic–pituitary–adrenal axis responsiveness and the monoaminergic system were significantly altered in pre-gestationally stressed offspring. Brain-derived neurotrophic factor (BDNF), cyclic adenosine monophosphate response element binding protein (CREB), phosphorylated CREB (pCREB), and serotonin transporter (SERT) protein levels were evaluated using western blotting with right hippocampus and right prefrontal cortex samples. Expression levels of BDNF, pCREB, and SERT in the offspring were also altered in the hippocampus and in the prefrontal cortex; however, there was no effect on CREB. We conclude that SDS before pregnancy might induce depressive-like behaviours, cognitive deficits, and neurobiological alterations in the offspring.

Chronic stress is a critical factor in the aetiology of anxiety disorders; however, in the clinic, enduring and preventive measures are not available, and therapeutic drugs are associated with inevitable side effects. Our study established an anxiety rat model using chronic restraint stress (CRS) and assessed these animals using the open‐field test, elevated plus‐maze test, and light‐dark box test. Jie‐Yu‐He‐Huan capsule (JYHH), a Chinese medicine formula, was used as a preventative drug. The HPA axis‐mediated release of corticotropin‐releasing hormone, adrenocorticotropic hormone, and corticosterone from the hypothalamus was tested. In the hippocampus and prefrontal cortex, concentrations of 5‐HT and its metabolite 5‐hydroxyindoleacetic acid, as well as monoamine oxidase A, glucocorticoid receptor, and 5‐HT1A receptor expression levels, were measured. Furthermore, we examined protein and mRNA expression of cAMP‐PKA‐CREB‐BDNF pathway components. The results showed that JYHH had a significant preventative effect on the anxiety‐like behaviour induced by CRS and prevented abnormal changes in the HPA axis and 5‐HT system. Furthermore, CRS inhibited the cAMP‐PKA‐CREB‐BDNF pathway, which returned to normal levels following JYHH treatment. This might be the underlying molecular mechanism of the antianxiety effect of JYHH, which could provide a new clinical target for preventative anxiolytic drugs for chronic stress.

Cadmium (Cd) is a toxic heavy metal that threatens public health, with kidney injury being one of the common manifestations after Cd exposure. Oxidative stress plays a crucial role in Cd-induced kidney injury, arising from an imbalance between cellular oxidation and antioxidation processes. Bromodomain-containing protein 4 (BRD4) has been identified as a significant factor in the initiation and advancement of multiple diseases, primarily due to its regulatory role in oxidative stress. Nevertheless, the specific role of BRD4 in Cd-induced kidney oxidative injury remains poorly understood. The present study demonstrates that BRD4 is activated in the kidney after Cd exposure, while JQ1 (a BRD4 inhibitor) treatment inhibits Cd-induced oxidative stress and kidney injury. Subsequently, we investigate the mechanisms by which Cd regulates oxidative stress both in vivo and in vitro. The results indicate that JQ1 treatment reduces the expression levels of NADPH oxidase 4 (Nox4), thereby alleviating mitochondrial damage and reducing reactive oxygen species (ROS) generation. Furthermore, JQ1 treatment facilitates nuclear translocation levels of Nuclear factor erythroid-derived 2-like 2 (Nrf2), thereby enhancing the antioxidant defense system in the kidney after Cd exposure. In conclusion, this study reveals that BRD4 is significantly involved in the process of Cd-induced oxidative damage in the kidney, while inhibiting BRD4 is observed to attenuate ROS generation by regulating Nox4 and enhance ROS scavenging by regulating Nrf2, which, in turn, suppresses the oxidative stress level in the kidney after Cd exposure. These findings suggest that targeting BRD4 may represent an effective strategy for the prevention and treatment of Cd-induced kidney diseases.

Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by motor dysfunction and non-motor symptoms, including cognitive decline. Animal models that replicate PD’s clinical features are essential for therapeutic research. The widely used subacute 1-methyl-4-phenyl-1,2,3,6tetrahydropyridine (MPTP)-induced mouse model effectively mimics motor deficits but fails to fully represent aging-related non-motor symptoms. In this study, we established an aging-associated PD mouse model by combining MPTP with D-galactose treatment. Compared to mice treated with MPTP alone, MPTP + D-galactose-treated mice exhibited typical motor impairments alongside cognitive deficits in the Morris water maze and Y-maze tests. D-galactose alone induced cognitive impairment without motor dysfunction. Pathological analysis showed that the MPTP + D-galactose treatment caused tyrosine hydroxylase-positive neuron loss similar to MPTP, while D-galactose did not damage these neurons. Additionally, Micro-CT revealed bone loss in both the MPTP + D-galactose and D-galactose groups. This model recapitulates both the motor and aging-related non-motor symptoms of PD, including cognitive impairment and bone loss, providing a more comprehensive tool for studying PD pathogenesis and evaluating potential therapies.