Cocoa Shell Extract Restores Redox Balance in Developmental Hypertension in Male Rats: Roles of Nrf2, SOD2 and p-eNOS

Area of Science:

• Biochemistry
• Physiology
• Pharmacology

Background:

• Hypertension is a global health issue linked to fetal malnutrition.
• Cocoa shell extract (CSE), a byproduct rich in antioxidants, is explored for its health benefits.
• Fetal malnutrition in male rats leads to hypertension and endothelial dysfunction, which CSE can ameliorate.

Purpose of the Study:

• To investigate the antioxidant mechanisms underlying the protective effects of CSE against hypertension and endothelial dysfunction induced by fetal malnutrition.
• To determine the impact of CSE on oxidative stress markers and related enzyme expressions in male and female offspring.

Main Methods:

• Adult male and female offspring from nutritionally restricted (fetal malnutrition) and control dams were supplemented with CSE or vehicle.
• Assessed plasma antioxidant enzyme activity (SOD), glutathione (GSH), and oxidative stress markers (carbonyls, 3-nitrotyrosine).
• Evaluated aortic expression of key enzymes involved in reactive oxygen species (ROS) production and degradation using Western blotting.

Main Results:

• Fetal malnutrition induced oxidative damage in male rat arteries, evidenced by increased carbonyls, SOD activity, SOD2, and phosphorylated-eNOS/eNOS, with reduced Nrf2 expression.
• Females showed elevated plasma SOD and aortic 3-nitrotyrosine.
• CSE supplementation reversed these detrimental effects, decreasing SOD2 and p-eNOS/eNOS, and increasing Nrf2 expression.

Conclusions:

• Arterial oxidative damage is a consequence of fetal malnutrition, with a more pronounced effect in males.
• Overexpression of SOD2 and p-eNOS/eNOS in malnourished rats may represent a compensatory response to increased superoxide anion production.
• CSE effectively mitigates vascular oxidative stress, likely via direct antioxidant action of its bioactive components.