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ABSTRACT: Background: Herbal medicines have been extensively used to treat coronavirus disease 2019 (COVID-19). Garlic, known to exert antiviral and anti-inflammatory effects, can be coadministered with standard treatments to combat COVID-19. Objectives: The aim of the study was to evaluate the efficacy and safety profile of Gallecina oral capsules (Samisaz Pharmaceutical Company, Mashhad, Iran), a fortified garlic extract, as adjunctive therapy to improve the clinical status and symptoms in noncritically ill patients hospitalized for COVID-19. Methods: This triple-blind randomized, placebo-controlled clinical trial was conducted on noncritically ill patients with COVID-19 hospitalized in the nonintensive care wards of Imam Hassan Hospital. Patients received remdesivir plus 90 mg Gallecina capsule or a placebo every 8 hours for 5 days or until discharge. The clinical status, respiratory symptoms, and laboratory parameters were recorded during the study period. Results: Patients were enrolled between April 24 and July 18, 2021. Data from 72 patients in the Gallecina group and 69 patients in the placebo group were analyzed. Oxygen saturation, C-reactive protein levels, and the distribution of respiratory distress and cough were similar between groups on the day of discharge. Although body temperature was significantly lower in the Gallecina group than that in the placebo group on the day of discharge (P = 0.04), it was within the normal range for both groups. The proportion of patients requiring supplemental oxygen for at least 1 day during the study was significantly reduced in the Gallecina group on days 3 and 4 and the day of discharge (P < 0.05). Gastrointestinal complaints were more prevalent in the Gallecina group than in the placebo group but the difference was not statistically significant (P = 0.12). Conclusions: There was no significant effect on the primary outcome of clinical status on study day 6. Although the proportion of Gallecina-treated patients who needed supplemental oxygen significantly decreased on days 3 and 4 and the day of discharge, there was no significant difference between the groups on other days. The possible beneficial effects on oxygen requirements in noncritically ill COVID-19 patients may warrant further investigation. (Curr Ther Res Clin Exp. 2023; 84:XXX–XXX). Clinical trial registration: IRCT20201111049347N1.

Abstract Statins are a family of drugs that are used for treating hyperlipidaemia with a recognized capacity to prevent cardiovascular disease events. They inhibit β‐hydroxy β‐methylglutaryl‐coenzyme A reductase, i.e. the rate‐limiting enzyme in mevalonate pathway, reduce endogenous cholesterol synthesis, and increase low‐density lipoprotein clearance by promoting low‐density lipoprotein receptor expression mainly in the hepatocytes. Statins have pleiotropic effects including stabilization of atherosclerotic plaques, immunomodulation, anti‐inflammatory properties, improvement of endothelial function, antioxidant, and anti‐thrombotic action. Despite all beneficial effects, statins may elicit adverse reactions such as myopathy. Studies have shown that mitochondria play an important role in statin‐induced myopathies. In this review, we aim to report the mechanisms of action of statins on mitochondrial function. Results have shown that statins have several effects on mitochondria including reduction of coenzyme Q10 level, inhibition of respiratory chain complexes, induction of mitochondrial apoptosis, dysregulation of Ca2+ metabolism, and carnitine palmitoyltransferase‐2 expression. The use of statins has been associated with the onset of additional pathological conditions like diabetes and dementia as a result of interference with mitochondrial pathways by various mechanisms, such as reduction in mitochondrial oxidative phosphorylation, increase in oxidative stress, decrease in uncoupling protein 3 concentration, and interference in amyloid‐β metabolism. Overall, data reported in this review suggest that statins may have major effects on mitochondrial function, and some of their adverse effects might be mediated through mitochondrial pathways.