Cytokine storm syndrome is a cascade of escalated immune responses disposing the immune system to exhaustion, which might ultimately result in organ failure and fatal respiratory distress. Infection with severe acute respiratory syndrome-coronavirus-2 can result in uncontrolled production of cytokines and eventually the development of cytokine storm syndrome. Mast cells may react to viruses in collaboration with other cells and lung autopsy findings from patients that died from the coronavirus disease that emerged in 2019 (COVID-19) showed accumulation of mast cells in the lungs that was thought to be the cause of pulmonary edema, inflammation, and thrombosis. In this review, we present evidence that a cytokine response by mast cells may initiate inappropriate antiviral immune responses and cause the development of cytokine storm syndrome. We also explore the potential of mast cell activators as adjuvants for COVID-19 vaccines and discuss the medications that target the functions of mast cells and could be of value in the treatment of COVID-19. Recognition of the cytokine storm is crucial for proper treatment of patients and preventing the release of mast cell mediators, as impeding the impacts imposed by these mediators could reduce the severity of COVID-19.

Objective: To determine whether captopril could prevent spinal cord damage after induction of ischemia-reperfusion injury in rats. Materials and Methods: We randomly divided 24 adult male Wistar rats, weighing 230 - 350 g, into 4 groups (n= 6 in each group): Spinal cord ischemia-reperfusion with captopril, spinal cord ischemia-reperfusion, sham operated with captopril, and SHAM. 24 and 1.5 hours before ischemia induction, captopril was administered intragastrically (100 mg/kg) to the SHAM+Cap and the SCI-R+Cap groups. Abdominal aortic clamping was performed in the SCI-R and SCI-R+Cap groups for 40 minutes. Hindlimb motor function was evaluated using the Tarlov Scale at 4, 6, 12, 24, 48, and 60 hours after SCI. Biomarkers of oxidative stress were measured to evaluate biological responses to therapeutic interventions (MDA, FRAP and PAB assays). Results: Throughout the study period, the SCI-R group had significantly lower motor function scores than the other groups (P < 0.05). The MDA and PAB levels were higher in the SCI-R group than in the SHAM group (P < 0.05). The FRAP value was lower in the SCI-R group than that in the SHAM group (P < 0.05). The SCI-R+Cap had higher motor function scores than the SCI-R group at all time points (P < 0.05). There were no notable differences in MDA concentration, FRAP and PAB values between the SCI-R+Cap and the SCI-R groups (P > 0.05). Conclusion: Captopril may act as a protective agent against spinal cord ischemia-reperfusion injury in rats based on hind limb motor function assessment.