Estrogen-mediated modulation of sterile inflammatory markers and baroreflex sensitivity in ovariectomized female Wistar rats.

Abstract

Objective: This study aims to explore the role of estrogen in providing cardioprotective benefits to premenopausal women, examining how hormonal differences between sexes influence the prevalence of cardiovascular diseases (CVDs) in women.

Materials and methods: Eighteen female Wistar rats were equally distributed into three treatment groups. Animals in Group I (sham-operated) and Group II (ovariectomized [OVX]) received oral saline solution at a dose of 2 mL/kg. Group III (OVX+E₂) received oral E₂ 2 µg/mL/kg after ovariectomy. Hemodynamic parameters and baroreflex sensitivity were determined in all groups. Plasma levels of malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) were measured, along with those of the inflammatory markers tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and high mobility group box-1 (HMGB-1).

Results: The OVX group, compared with the sham-operated group, displayed significantly altered hemodynamic parameters and baroreflex sensitivity, along with elevated MDA levels and decreased SOD and NO levels. This group also had higher levels of inflammatory cytokines than the sham-operated group. In the absence of estrogen, these factors led to the advancement of cardiovascular abnormalities. In the OVX+E₂ group, estrogen treatment considerably improved baroreflex sensitivity and hemodynamic profile while reducing the expression of inflammatory cytokines compared with the OVX group, demonstrating anti-inflammatory actions of estrogen.

Conclusion: Estrogen mediates cardioprotection by improving baroreflex sensitivity in ovariectomized Wistar rats through modulation of the NO pathway.