The effect of angiotensin receptor type 2 inhibition and estrogen on experimental traumatic brain injury

Background: Estrogen interferes with renin-angiotensin system (RAS). Increasing evidence suggests that estrogen interferes with the RAS such as decreasing angiotensin receptor in the brain. Objectives: This study aimed at investigating the mutual interaction between estrogen and candesartan (an angiotensin receptor blocker) to inhibit or amplify each other's neuroprotective effects after traumatic brain injury (TBI). Materials and Methods: Female rats were divided into 11 groups and the ovaries were removed in nine groups. Study groups included sham, TBI, oil, vehicle (Veh), a low dose (LC) and a high dose (HC) of candesartan, estrogen (E2), Veh + Veh, and a combination of estrogen with a low dose (E2 + LC) and a high dose (E2 + HC) of candesartan. TBI was induced by the Marmarou's method. Brain edema and integrity of blood brain barrier (BBB) were assayed by calculating brain water content (BWC) and Evans blue content, respectively. The neurological outcome was evaluated using the veterinary coma scale (VCS). Results: The results showed that the BWC in the E2 group was less than that of the oil group (P P P P P P Conclusion: Prescribing estrogen alone and a high dose of candesartan and a low dose of candesartan with estrogen has a neuroprotective effect on brain edema, permeability of BBB, and neurological scores. This may suggest that estrogen and candesartan (especially in a low dose) act via similar paths