RESUMEN
The current study was designed to explore the effect of fermented camel milk, plant sterols and their combination on the blood levels of sd-LDL and atherogenicity in rats fed on high-fat-cholesterol diets (HFC). Forty male Wistar rats were distributed into five groups: Normal control (NC), Positive control (PC, HFC), plant sterol (PS, HFC containing 1% (w/w) ß-sitosterol:Stigmasterols; 9:1), FM (HFC containing 4% (w/w) lyophilized fermented camel milk), and PSFM (HFC containing 1% (w/w) plant sterols +4% (w/w) lyophilized fermented camel milk). Antioxidant activity showed that ß-sitosterol had the highest radical scavenging activity, followed by fermented camel milk and stigmasterol (p < 0.05). Feeding rats on HFC for 8 weeks resulted in a significant (p < 0.05) increase in blood lipids of PC group compared with NC group. Administration of PS, FM, and PSFM resulted in a significant reduction in atherogenic index (50, 24.5, and 41.5 %, p < 0.05), and sd-LDL levels (73, 45, and 59%, p < 0.05), respectively. Only the FM group showed a significant reduction in triglycerides levels of rats. Administration of PS, FM and PSFM decreased serum MDA levels significantly by 58.7, 45.4, and 69% (p < 0.05), and increased total antioxidant capacity by 35.9, 84.8, and 38.3% (p < 0.05), respectively. This is the first report to the best of our knowledge that shows fermented camel milk enriched with plant sterol could reduce atherogenesis and cardiovascular diseases activity via inhibition of the status of small dense LDL and oxidative stress.
RESUMEN
Mucormycosis (MCM) is a rare fungal disorder that has recently been increased in parallel with novel COVID-19 infection. MCM with COVID-19 is extremely lethal, particularly in immunocompromised individuals. The collection of available scientific information helps in the management of this co-infection, but still, the main question on COVID-19, whether it is occasional, participatory, concurrent, or coincidental needs to be addressed. Several case reports of these co-infections have been explained as causal associations, but the direct contribution in immunocompromised individuals remains to be explored completely. This review aims to provide an update that serves as a guide for the diagnosis and treatment of MCM patients' co-infection with COVID-19. The initial report has suggested that COVID-19 patients might be susceptible to developing invasive fungal infections by different species, including MCM as a co-infection. In spite of this, co-infection has been explored only in severe cases with common triangles: diabetes, diabetes ketoacidosis, and corticosteroids. Pathogenic mechanisms in the aggressiveness of MCM infection involves the reduction of phagocytic activity, attainable quantities of ferritin attributed with transferrin in diabetic ketoacidosis, and fungal heme oxygenase, which enhances iron absorption for its metabolism. Therefore, severe COVID-19 cases are associated with increased risk factors of invasive fungal co-infections. In addition, COVID-19 infection leads to reduction in cluster of differentiation, especially CD4+ and CD8+ T cell counts, which may be highly implicated in fungal co-infections. Thus, the progress in MCM management is dependent on a different strategy, including reduction or stopping of implicit predisposing factors, early intake of active antifungal drugs at appropriate doses, and complete elimination via surgical debridement of infected tissues.
