Spicing Up the Rostral Ventrolateral Medulla: Immunohistochemical Analysis of Curcumin's Effects on Brainstem Pathways in Obesity-Induced Hypertension
Description
Obesity and post menopause augments the development of hypertension independently and collectively in women. Unfortunately, hypertensive medications have been described to work in approximately 30% of hypertensive patients, warranting the need for alternative approaches to treat this disease. Curcumin is a natural compound with antioxidant and anti-inflammatory properties; this extract is derived from turmeric, and has been shown in our lab and others to have the capacity to lower blood pressure. However, the mechanism(s) by which curcumin has this effect is incompletely understood. Identifying these mechanism(s) can play an essential role in developing targeted therapeutic interventions that may one day mitigate hypertension in post-menopausal and obese patients. We tested the hypothesis that curcumin could block the activation of glutamatergic (i.e., excitatory) neurons in the RVLM (rostral ventrolateral medulla) by blocking the phosphorylation of NMDA receptors (pNMDAR) in obese mice and obese female mice that are estrogen deficient. Brains from perfused animals were sectioned thirty microns thick throughout the hindbrain and processed at the same time to ensure uniformity of immunostaining. Histological expressions of VGLUT and pNMDAR were identified in the RVLM. We observed that in obese premenopausal (i.e., estrogen-replete) mice, curcumin did not block the pNMDAR. However, it did in our obese postmenopausal mouse model. Furthermore, we observed a significant decrease in blood pressure only in our postmenopausal mouse model that consumed curcumin. These data suggest that curcumin decreases blood pressure, in part, by regulating the activity of neurons in cardio regulatory sites (i.e. RVLM) in the central nervous system.
Citation Information
Sanchez-Tarre, Stephania; Bunge, Tatiana; and Barnes, Maria J., "Spicing Up the Rostral Ventrolateral Medulla: Immunohistochemical Analysis of Curcumin's Effects on Brainstem Pathways in Obesity-Induced Hypertension" (2026). Office of Research DMU Research Symposium. 72.
https://digitalcommons.dmu.edu/researchsymposium/2025rs/2025abstracts/72
Spicing Up the Rostral Ventrolateral Medulla: Immunohistochemical Analysis of Curcumin's Effects on Brainstem Pathways in Obesity-Induced Hypertension
Obesity and post menopause augments the development of hypertension independently and collectively in women. Unfortunately, hypertensive medications have been described to work in approximately 30% of hypertensive patients, warranting the need for alternative approaches to treat this disease. Curcumin is a natural compound with antioxidant and anti-inflammatory properties; this extract is derived from turmeric, and has been shown in our lab and others to have the capacity to lower blood pressure. However, the mechanism(s) by which curcumin has this effect is incompletely understood. Identifying these mechanism(s) can play an essential role in developing targeted therapeutic interventions that may one day mitigate hypertension in post-menopausal and obese patients. We tested the hypothesis that curcumin could block the activation of glutamatergic (i.e., excitatory) neurons in the RVLM (rostral ventrolateral medulla) by blocking the phosphorylation of NMDA receptors (pNMDAR) in obese mice and obese female mice that are estrogen deficient. Brains from perfused animals were sectioned thirty microns thick throughout the hindbrain and processed at the same time to ensure uniformity of immunostaining. Histological expressions of VGLUT and pNMDAR were identified in the RVLM. We observed that in obese premenopausal (i.e., estrogen-replete) mice, curcumin did not block the pNMDAR. However, it did in our obese postmenopausal mouse model. Furthermore, we observed a significant decrease in blood pressure only in our postmenopausal mouse model that consumed curcumin. These data suggest that curcumin decreases blood pressure, in part, by regulating the activity of neurons in cardio regulatory sites (i.e. RVLM) in the central nervous system.
