The Common Myrtle (Myrtus communis L.) is rich in antioxidants, particularly in anthocyanin. It was recognized for its anti-inflammatory and anti-thrombotic effects.

The aim of our work is to evaluate the effect of Common Myrtle on a model of hepatic ischemia-reperfusion in Rat.

Two morphs were chosen: white fruit Myrtle and black fruit Myrtle. Within each morph, fruit and leaf were separated and obtained extract were used to determine their effects on the hepatic model of ischemia-reperfusion.

Our work was conducted in three steps (1) Induction of hepatic ischemia (90 minutes) in Wistar Rat (2) injection of the Myrtle extract during 15 minutes before reperfusion (3) and reperfusion (2 hours).

To evaluate the effect of Myrtle on ischemia-reperfusion, we have monitored transaminases levels, Monoethylglycinexylidide (MEGX) concentrations (to assess the liver metabolic capacity) and Malondialdehyde (MDA) concentration.

The determination of total phenol extracts of Myrtle showed a significant difference between black fruit Myrtle (11.3 μg/ml), white fruit (27 μg/ml) and black fruit Myrtle leaves (94.3 μg/ml). The latter presented the highest antioxidant activity (86.54%).

With the extract from the white fruit of Myrtle, we noted a decrease of AST and ALT, respectively, 1321 U/I and 773 U/I compared with I/R group was 5757 U/I and 5404 U/I and an increase in the MEGX concentrations and decrease in MDA.

The testing of extracts of Myrtle in a model of hepatic ischemia showed a difference in the protective power against damage of ischemia-reperfusion, by origin and type of fruit (black or white).

Transplantation of solid organs is invariably linked to a disruption of oxygen and nutrient supply. Damage initiated in the ischemic period is greatly enhanced during reperfusion. In particular the excessive production of reactive oxygen species (ROS) plays a key role in the development of ischemia/reperfusion injury (IRI), which in the clinical setting is difficult to control through the use of antioxidants. Ischemia/reperfusion (IR) is also marked by the activation of intracellular signaling pathways, which may have protective but also damaging effects. Modulating intracellular signaling thus may hold the promise to prevent or minimize IRI. Most intriguingly, some of these pathways have been shown recently to control mitochondrial events, including the production of ROS. Understanding this cytoplasmic/ mitochondrial crosstalk will be the basis for the development of novel approaches for the prevention of IRI.

Orthotopic liver transplantation is the only treatment for end stage liver disease. Recipients outweigh the number of available healthy donor livers, and options for increasing the donor pool have included the use of marginal livers. Transplantation of marginal livers is a known risk factor for the development of primary non-function post-transplant. Although the precise cause of primary non-function is not known, ischemia/reperfusion (I/R) injury has been strongly implicated, and tumor necrosis factor-α (TNF-α) plays a critical role. We utilized a rat I/R model to determine whether treatment with tissue inhibitor of metalloproteinase-3 (TIMP-3) after total sublethal I/R injury improves liver health by preventing the release of active TNF-α. Rats were pre-treated with either TIMP-3 or saline and underwent total warm hepatic ischemia followed by 6, 24, 48 hours or 7 days reperfusion. All rats survived treatment and I/R injury. Serum samples were assayed for TNF-α, interleukin-6 (IL-6), and alanine aminotransferase (ALT). Histology and RT-PCR for TNF-α and TNF-α-converting enzyme [TACE or a disintegrin and metalloproteinase-17 (ADAM-17)] were performed on liver tissues. TIMP-3 treatment resulted in decreased TNF-α and IL-6 levels, and the inhibition occurred at a posttranscriptional level as mRNA expression of TNF-α and TACE/ADAM-17 was not affected. ALT levels reached basal levels in TIMP-3-treated rats more quickly than untreated rats, and livers of treated rats showed mild edema while livers of untreated rats exhibited hepatic collapse, necrosis, and hemorrhage. Our results indicate that TIMP-3 treatment protects the liver from total sublethal I/R injury through a TNF-α-specific pathway. 

Reconstructive transplantation, also referred to as vascularized composite allotransplantation (VCA), has rapidly emerged as a viable approach to repairing complex tissue defects. Over the past 20 years, major advances have been made in the field of VCA allowing for successful transplantation of over 150 hand/forearm/arm, larynx, trachea, abdominal wall, vascularized knee, and facial transplants with encouraging outcomes. These innovations have currently outpaced the scientific community’s ability to fully address certain immunological and clinical challenges. The literature on ischemia-reperfusion injury (IRI) in VCA is limited and mechanistic questions remain. Specifically, the role IRI may play in acute rejection, the progression towards chronic rejection, or immune regulation and tolerance induction has only been partially or indirectly addressed. Hence, much of what we understand regarding IRI in VCA is extrapolated from research in solid organ transplantation (SOT). This review will address the role of IRI in VCA, first outlining its impact on SOT, it’s effects on the immune system and allograft rejection, as well as the clinical implications that IRI has for VCA outcomes.