Melamine (ML), a chemical substance of high nitrogen content, is used as a food adulterant. Former evidences implied that ML could induce a variety of toxic effects including neurotoxicity and cognitive impairment. Therefore, the aim of this study was to delineate the protective effect of the nootkatone (NK) against ML-induced neural adverse effects. Rats were orally pretreated with NK (5 and 10 mg/kg) prior to the oral administration of ML (700 mg/kg) for a period of 28 days. Our findings unveiled remarkable alleviating effect of NK on MK-induced neurobehavioral disturbance in open field test. Furthermore, NK lessened ML-caused increases in the acetylcholine esterase level in the brain tissue of exposed rats. NK also decreased the neural oxidative stress as represented by elevated levels of SOD, CAT, and GSH along with decreased MDA and NO levels. Upregulated mRNA expression levels of neural NRF-2 and HO-1 were noticed after NK administration. Remarkable anti-inflammatory impact was prominent by decreased neural IL-1β, and TNF-α along with downregulated NF-κB and TLR-4 gene expression levels in NK-treated rats. Noteworthily, pre-treatment with NK decreased the immune reaction of RAGE and HMGB-1 induced by oral ML exposure. Brain histological examination validated the obtained biochemical and molecular results. To sum up, these outcomes reveal that NK successfully alleviated the neural damage induced by ML via blocking of oxidative stress, and inflammatory signaling pathways. Consequently, our study may suggest NK as a new effective therapeutic supplement for treatment of ML-mediated neurotoxicity in rats via inhibition of HMGB-1-RAGE/TLR-4/NF-κB.

Objectives: Present report evaluates the protective effect of geraniol on high fat diet (HFD) induced obesity in rats and also determines the molecular mechanism of it. Methods: Rats were induced with obesity with administration of HFD for four weeks and geraniol 200 and 400 mg/kg p.o. was administered for the next four week in the respective groups. Blood glucose and oral glucose tolerance test (OGTT), lipid profile was estimated in the geraniol treated HFD induced obesity in rats. Moreover, docking study was performed to determine the specific mechanism of geraniol by targeting HMG-CoE A reductase (in silico). Results: There was significant increase in body weight and amelioration in altered serum glucose and lipid profile were observed in the geraniol treated group than negative control group. Weight of organs and adipose tissue isolated from different regions of the body was reduced in geraniol treated group than negative control. Moreover, geraniol interact with HMG-CoA reductase having binding energy −5.13. Conclusions: In conclusion, data of the report reveals that geraniol reduces obesity by promoting the conversion of white adipose tissue (WAT) to brown adipose tissue (BAT), as it interacts with HMG-CoA reductase in HFD induced obesity in rats.

This study examines the histological, ultrastructural, and immunohistochemical features of the lip skin of the goldfish (Carassius auratus, Linnaeus, 1758), a sensory-rich region that plays an essential role in feeding and environmental perception. Our findings highlight the coexistence and close association of immune, epithelial, and sensory cells within the epidermis and dermis. For the first time in goldfish, intraepidermal macrophages, eosinophilic granular cells, rodlet cells, Merkel cells, and several specialized sensory structures—neuromasts, taste buds, and tuberous-like sensory units—were simultaneously identified within the same integumentary field. Quantitative morphometry demonstrated a high density of eosinophilic granular cells, rodlet cells, and neuromasts per unit epithelial area, reinforcing the functional specialization of the goldfish lip as a sensory–immune interface. Immunohistochemical markers (CK20, S100, CD68, CD64, CD117, and E-cadherin) were applied as complementary tools to describe phenotypic labeling patterns. These findings are interpreted cautiously as supportive evidence consistent with epithelial, neural-associated, stromal, and immune cell distributions observed morphologically. Transmission electron microscopy further uncovered fine structural details such as synapse-like contacts in taste buds and Merkel cells, dense-core granules in eosinophilic granular cells, and telocyte–nerve fiber associations in the dermis. By integrating cellular, structural, and immunohistochemical perspectives, this study provides a novel descriptive reference for the goldfish lip skin as a region characterized by the close spatial association of sensory and immune-related elements, underscoring its value as a model for vertebrate cutaneous biology and neuroimmunology.

An excess of calories impairs visceral adipose tissue functioning, including heart adipose and perivascular-adipose-tissue (PAT). The secretory activity of adipose tissue (AT), which encompasses both pro-inflammatory and endocrine mediators, plays a pivotal role in inter-organ communication and contributes significantly to the pathogenesis of obesity. Excessive fat in visceral adipocytes hinders the endocrine and immunological response, resulting in pathological alterations and presenting significant threats to human health risk. Previous research has established that increased pro-inflammatory cytokines and decreased immune-modulatory disrupt the communication between vasculature, liver, and myocyte. Adiposopathy or dysfunctional AT contributes to the development of cardio-metabolic-risk factors (CMRF). These risk factors include metabolic resistance, hypertension, dyslipidemia, atherosclerosis, and a hypercoagulable state. These risk factors consecutively, unswervingly, and circuitously contribute to the growth of cardiometabolic disorders. The perivascular adipose tissue envelops most blood arteries throughout the body. Functional PAT has anticontractile and immune-modulatory properties. However, it has been proposed that impaired PAT activity may contribute to the association between CMRF and vascular dysfunction. Vascular oxidative stress is a critical contributor to the progression of cardiometabolic disorders associated with obesity, type 2 diabetes, and hypertension. Increasing evidence from both human and animal studies suggests that physical exercise supports the normalization of adipocyte size and promotes the browning of white adipose tissue (WAT). This review covers the existing studies concerning the impact of adiposopathy on cardiometabolic disorders and the significance of physical activity in reinstating adipocyte function. Additionally, it explores the processes that connect PAT to age-related vascular pathologies.