Our laboratory has observed that curcumin, a bioactive compound derived from turmeric with anti-inflammatory properties, can lower blood pressure in an obese postmenopausal mouse model. However, the mechanism(s) by which curcumin mediated this physiological response is unknown. In this study, we tested the hypothesis that curcumin can mimic estrogenic actions by decreasing the phosphorylation of N-methyl-D-aspartate receptors (p-NMDAR), thereby modulating glutamatergic or GABAergic pathways involved in blood pressure regulation. Male (n=4) and female mice that were estrogen replete (SHAM; n=4) or depleted of estrogen (OVX; n=4) developed obesity after ad libitum consumption of a 60% high-fat diet. Female mice were ovariectomized or underwent a sham surgery. After seven days of recovery, mice received a daily gavage of 300 mg of curcumin or the control treatment (i.e., piperine) for thirty days. Mice were anesthetized, and the hypothalamus was extracted for isolation of protein. Western blot analysis assessed changes in p-NMDAR expression, normalized to β-actin. Obesity in both groups of female mice significantly increased p-NMDAR expression (SHAM: p=0.0389; OVX: p=0.0003). Curcumin treatment significantly decreased p-NMDAR expression in the hypothalamus of OVX mice (p=0.001). However, curcumin treatment did not alter the phosphorylation of NMDA receptors in the SHAM females or the male mice. These data suggest that curcumin could potentially mimic the actions of estrogen to lower blood pressure by regulating the activity of NMDA receptors in the central nervous system. Supported by Iowa Osteopathic Educational Research Foundation Grant Number: 06-24-02. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Crowl et al. (Fri,) studied this question.