Abstract
Heat stress induces the hypothalamic-pituitary-adrenal (HPA) axis activation, influences biological responses, and reduces energy metabolism. Geongangbuja-tang (GBT) and its components, Zingiberis Rhizoma (ZOR) and Aconiti Lateralis Radix Preparata (ALRP) have been used to induce energy metabolism; however, the effects of GBT and its ingredients on heat-induced inflammatory responses have not yet been investigated. In this study, we performed an open-field test to evaluate locomotor activity in mice. To assess the effects of GBT and its ingredients on inflammation, the protein levels of c-fos, pro-inflammatory cytokines, and cortisol were measured in the mouse hypothalamus and serum. The results showed that GBT alleviated locomotive activity and reduced c-fos levels in a dose-dependent manner under the heat exposure. After investigating the active constituent of GBT, we found that compared to GBT and ZOR, ALRP significantly suppressed c-fos expression under heat stress. Subsequently, ALRP decreased the expression of pro-inflammatory cytokines, such as interleukin-9 and -13 and prostaglandin, under the heat stress in the mouse hypothalamus. Moreover, treatment with ALRP inhibited cortisol secretion in the mouse serum following heat exposure. These results indicate that GBT and its active component, ALRP, could be the thermoregulatory agents that regulate the HPA axis.
Highlights
As global temperature has been gradually rising, the issue of pathophysiological responses in living organisms has been raised
To evaluate the effects of Aconiti Lateralis Radix Preparata (ALRP) on PGE levels in the hypothalamus, we examined the ratio of PGE2 to prostaglandin E 1 (PGE1) using enzyme-linked immunosorbent assay (ELISA), and found it to be significantly upregulated after heat exposure (113 ± 3% of control); this ratio was significantly restored by ALRP at 300 mg/kg/day (100 ± 5%, Figure 4C)
To reveal the anti-inflammatory effects of ALPR against heat stress, we demonstrated the downregulation of levels of IL-9, IL-13, PGE1, and PGE2 levels in the mouse hypothalamus, which resulted in the secretion of cortisol in mice
Summary
As global temperature has been gradually rising, the issue of pathophysiological responses in living organisms has been raised. Heat stress has been reported to be a critical factor causing hyperthermia, anorexia, weight loss, hypoglycemia, gastric hemorrhage, spermatogenesis dysfunction, heatstroke, and neurological disorders [1,2] These symptoms result from systemic metabolic disorders induced by reduced food intake and hormone secretion levels. The HPA axis, which includes the autonomic nervous system, plays a crucial role in regulating metabolic dysregulation by thermal stress in response to stressful stimuli, which can self-activate through neurotransmitters [4] Hormones, such as glucocorticoids and corticosterone, are controlled by the HPA axis and secreted in response to stress, which results in suppression of the systemic immune response and stimulation of pro-inflammatory cytokines [5]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
