Protective Effect of Thymosin β4 against Abdominal Aortic Ischemia–Reperfusion-Induced Acute Lung Injury in Rats

Abstract

Background and objectives: Ischemia–reperfusion (IR) caused by infrarenal abdominal aorta cross-clamping is an important factor in the development of ischemia–reperfusion injury in various distant organs. Materials and Methods: We investigated potential antioxidant/anti-inflammatory effects of thymosin beta 4 (Tβ4) in a rat model of abdominal aortic surgery-induced IR. Tβ4 (10 mg/kg, intravenous (i.v.)) was administered to rats with IR (90-min ischemia, 180-min reperfusion) at two different periods. One group received Tβ4 1 h before ischemia, and the other received 15 min before the reperfusion period. Results: Results were compared to control and non-Tβ4-treated rats with IR. Serum, bronchoalveolar lavage fluid and lung tissue levels of oxidant parameters were higher, while antioxidant levels were lower in the IR group compared to control. IR also increased inflammatory cytokine levels. Tβ4 reverted these parameters in both Tβ4-treated groups compared to the untreated IR group. Conclusions: Since there is no statistical difference between the prescribed results of both Tβ4-treated groups, our study demonstrates that Tβ4 reduced lung oxidative stress and inflammation following IR and prevented lung tissue injury regardless of timing of administration.

Resveratrol against lung injury in an ischemia/reperfusion model of abdominal aortic rupture

“…[ 4 ] The I /Rep has been reported to cause a significant increase in MDA levels in lung tissues in studies involving clamping of the IAA and in studies involving pulmonary hilus clamping. [ 4 , 14 , 16 , 17 , 20 ] Similarly, in the present study, and consistent with previous research, we observed that I/Rep increased the lung tissue MDA levels.…”

“…[ 15 - 17 ] Additionally, Kurt et al[ 17 ] observed edema and hyaline cast structures in transition areas of the respiratory bronchioles, dilatation in the saccus alveolaris, edema in the subepithelial bronchial region, as well as irregularity in the lamina propria, perivascular edema, and obstruction in small capillary vessels as a result of I/Rep at examination of pulmonary tissues. Yaman et al[ 16 ] recorded swelling and vacuolization in the bronchial epithelium, increased pulmonary vascular permeability, and dilatation in the alveoli. They also observed that interstitial edema and inflammatory cell inflammation caused capillary obstruction, and thickening of and damage to the alveolar wall in some regions.…”

“…Additionally, the release of proteolytic enzymes as a result of neutrophil adhesion to the endothelium and the activation of caspase-3 enzyme systems results in apoptosis and lung cell death. [ 16 - 18 ] Kurt et al[ 17 ] determined that I /Rep induced by occlusion of the IAA exacerbated the activity of caspase-3 and increased the incidence of apoptosis in pulmonary cells. Wang et al[ 18 ] also reported significant increases in caspase-3 enzyme content, apoptotic cells, and cell death in lung tissue with I/Rep.…”

“…[ 19 ] The ROS lead to increased cell permeability and lysis by causing lipid peroxidation in the cell membrane. [ 16 ] As one of the end products of I/Rep injury, MDA emerges with the breakdown of polyunsaturated fatty acids. It provides reliable information about the every of the peroxidation reaction and tissue damage, and is used as a marker in determining oxidative damage.…”

“…Determination of GSH and CAT levels is used to gain insight into the severity of oxidative stress exposed. [ 15 , 16 ] Yaman et al[ 16 ] reported depletion of endogenous GSH due to I/Rep and low GSH levels in lung tissue in I/Rep group. Kumbasar et al[ 4 ] reported significant decreases in both GSH and CAT levels in lung tissue after I/Rep.…”