Mannose binding lectin is a lectin instrumental in the innate immunity. It recognizes carbohydrate patterns found on the surface of a large number of pathogenic micro-organisms, activating the complement system. However, this protein seems to increase the tissue damage after ischemia. In this paper is reviewed some aspects of harmful role of the mannose binding lectin in ischemia/reperfusion injury.
Some studies have shown that statins have a promising effect on protection against reperfusion injury.
To evaluate the ability of ischemic postconditioning, statins and both associated to prevent or minimize reperfusion injury in the liver of rats subjected to ischemia and reperfusion by abdominal aorta clamping.
Were used 41 Wistar rats, which were distributed into five groups: ischemia and reperfusion (I/R), ischemic postcondictioning (IPC), postconditioning + statin (IPC+S), statin (S) and Sham. It was performed a medium laparotomy, dissection and isolation of the infra-renal abdominal aorta; excepting Sham group, all the others were submitted to the aorta clamping for 70 min (ischemia) and posterior clamping removing (reperfusion, 70 min). In the IPC and IPC+S groups, postconditioning was performed between the ischemia and reperfusion phases by four cycles of reperfusion and ischemia lasting 30 s each. In IPC+S and S groups, preceding the surgical procedure, administration of 3.4 mg/day of atorvastatin was performed for seven days by gavage. The left hepatic lobe was removed for histological study and euthanasia was performed.
The mean hepatic injury was 3 in the I/R group, 1.5 in the IPC group, 1.2 in the IPC+S group, 1.2 in the S group, and 0 in the SHAM group. The I/R group had a higher degree of tissue injury compared to the others in the statistical analysis and there was no difference between the others (p<0.01).
Ischemic postconditioning and atorvastatin were able to minimize hepatic reperfusion injury, either alone or in combination.
It is currently understood that severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) directly enters target cells by binding to the angiotensin-converting enzyme 2 (ACE2) receptor. Accordingly, tissues with high expression levels of ACE2 are more susceptible to infection, including pulmonary alveolar epithelial cells, small intestine enterocytes, cholangiocytes, and vascular endothelial cells. Considering the atypical manifestations of COVID-19 and the challenges of early diagnosis, this review addresses the possible gastrointestinal complications of the disease.
The phrase “Gastrointestinal complication of COVID” was searched in the PubMed, Medline, and SciELO databases. Due to the heterogeneity of the studies included in the present review, a narrative synthesis of the available qualitative data was performed.
The literature search retrieved 28 articles, primarily case reports and case series, for the qualitative analysis of gastrointestinal complications of COVID-19, in addition to two retrospective cohort and one case-control. The studies focused on hemorrhagic, thrombotic, ischemic, and perforation complications, in addition to acute pancreatitis and pneumatosis intestinalis.
There is a straight relationship between high expression levels of ACE2 in the gastrointestinal tract and its greater susceptibility to direct infection by SARS-CoV-2. So, it is important to consider the gastrointestinal infection manifestations for early diagnosis and treatment trying to avoid more serious complications and death.
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