Acute mesenteric ischemia (AMI) is a life-threatening condition characterised by oxidative
stress, inflammation, apoptosis, and necrosis of intestinal epithelial cells. Different drugs
with vasoactive, antioxidant, and anti-inflammatory properties have been used to treat
AMI. Levosimendan is a drug with proven anti-ischemic effects used in the management of
acute congestive heart failure. This study evaluated the protective effects of levosimendan
pretreatment on intestinal, as well as lung, heart, and kidney tissue in a rat model of mesenteric artery ischemia/reperfusion (I/R) injury. Male Wistar rats (N = 24) were divided
into four groups: control, I/R, levosimendan (LS) 1 mg/kg i.p, and LS + I/R (1 mg/kg
i.p. 30 min before injury). I/R by itself caused elevation of oxidative markers (thyobarbituric acid reactive species (TBARS), hydrogen peroxide (H2O2), super oxide anjon radical
(O2
−), and nitrogen dioxide (NO2
−)), induced inflammation (macrophage infiltration and
Interleukin-6 (IL-6) production), and apoptosis (nuclear factor kappa light-chain enhancer
of activated B cells (NF-κB), cleaved caspase-3 (CC3), and terminal deoxy-nucleotidyl transferase (TdT)-mediated dUTP nick end labelling (TUNEL)). Levosimendan pretreatment
significantly reduced oxidative stress markers and enhanced antioxidant defences (catalase
(CAT), reduced glutathione (GSH), and superoxide dismutase (SOD)). Histological analysisrevealed reduced mucosal damage and preserved goblet cells in intestinal tissue. Similar
protective effects of levosimendan were observed in other organs such as lung, heart, and
kidney. Immunohistochemistry showed reduced epithelial apoptosis and upregulation
of antioxidant and anti-inflammatory proteins. These findings highlight levosimendan’s
ability to protect mesenteric I/R tissue injury and multi-organ damage by suppressing
oxidative stress, inflammation, and apoptosis, emphasising its therapeutic potential in
clinical settings
