Postmenopausal women experience estrogen deficiency-related menopausal symptoms (e.g., hot flashes and mood swings) and a dramatic increase in the incidence of chronic diseases. Although estrogen-replacement therapy (ERT) can reduce mortality from cardiovascular disease and improve osteoporosis and menopausal symptoms, its side effects have limited recent use. This study investigated the estrogen-like activity of aqueous extract from Agrimonia pilosa Ledeb.

Estrogen deficiency is associated with obesity, dyslipidemia, and increased insulin resistance in postmenopausal women. An efficient therapeutic agent prevents or improves postmenopausal conditions induced by estrogen deficiency. Here, we investigated the effects of aqueous Agrimonia pilosa Ledeb. extract on glucose and lipid metabolism in ovariectomized rats fed a high-fat diet (HFD). Female Sprague-Dawley rats were sham-operated or ovariectomized, and 3 weeks later were assigned to the following groups: sham-operated + HFD (S); ovariectomized + HFD (OVX); and ovariectomized + HFD with 0.5% A. pilosa aqueous extract (OVX + 0.5A) groups. Ovariectomy significantly increased body weight and dietary intake relative to the S group. However, A. pilosa treatment did not significantly affect weight gain or dietary intake. Blood triacylglycerol, total cholesterol, and low-density lipoprotein cholesterol levels tended to decrease in the A. pilosa-supplemented group. Blood glucose levels were significantly lower in the OVX + 0.5A group than those in the OVX group. Blood adiponectin and insulin concentrations increased significantly after A. pilosa treatment in the ovariectomized group. A. pilosa supplementation tended to decrease liver weights and prevented lipid accumulation. These effects correlated with reduced hepatic expression of lipogenesis-related genes (fatty acid synthase, acetyl-coenzyme A carboxylase alpha, and 3-hydroxy-3-methylglutaryl-coenzyme A reductase). Therefore, A. pilosa may improve metabolic disorders in ovariectomized rats.

The control of exosome release is associated with numerous physiological and pathological activities, and that release is often indicative of health, disease, and environmental nutrient stress. Tuberous sclerosis complex (TSC) regulates the cell viability via the negative regulation of the mammalian target of rapamycin complex (mTORC1) during glucose deprivation. However, the mechanism by which viability of TSC-null cells is regulated by mTORC1 inhibition under glucose deprivation remains unclear. Here, we demonstrated that exosome release regulates cell death induced by glucose deprivation in TSC-null cells. The mTORC1 inhibition by rapamycin significantly increased the exosome biogenesis, exosome secretion, and cell viability in TSC-null cells. In addition, the increase in cell viability by mTORC1 inhibition was attenuated by two different types of inhibitors of exosome release under glucose deprivation. Taken together, we suggest that exosome release inhibition might be a novel way for regression of cell growth in TSC-null cells showing lack of cell death by mTORC1 inhibition.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interactions, communication deficits, and excessive repetitive behaviors. While ASD has a strong genetic basis, growing evidence suggests that epileptic seizures may serve as environmental risk factors for ASD development. The high comorbidity between epilepsy and ASD (20–30%) suggests potential shared neurobiological mechanisms, yet the causal relationship remains poorly understood. To investigate the causal role of seizures in the development of ASD-like pathology, we exposed adolescent mice (3 weeks old) to electroconvulsive seizures (ECS) for 10 consecutive days. This repeated ECS exposure led to the emergence of autistic-like behaviors including significantly decreased sociability, increased repetitive self-grooming, enhanced marble burying behavior, and anxiety-like behaviors, without affecting general locomotor activity. Additionally, repeated exposure to ECS induced significant changes in glutamatergic neurotransmission in the mice’s prefrontal cortex and hippocampus, brain regions critically involved in social cognition and behavioral regulation. Interestingly, these changes occurred without alterations in other excitatory/inhibitory neuronal markers, suggesting a specific impact on glutamate receptor expression rather than a general disruption of excitatory/inhibitory balance. These findings suggest that repeated seizures may contribute to ASD-like symptoms by specifically affecting key glutamatergic neurotransmitter systems, providing insights into the neurobiological mechanisms underlying the comorbidity between epilepsy and autism. In addition, repeated ECS differentially regulated histone deacetylase (HDAC) transcripts in a region-specific manner and produced seizure-intensity-dependent transcriptomic signatures.