Inhibition of poly(ADP-ribose) polymerase attenuates lung tissue damage after hind limb ischemia-reperfusion in rats

The protective effects of curcumin on intestine and remote organs against mesenteric ischemia/reperfusion injury

“…Lung injury was evaluated using an ordinal scale as follows: grade 0 = no change; grade 1 = mild neutrophil leukocyte infiltration and mild to moderate interstitial congestion; grade 2 = moderate neutrophil leukocyte infiltration, perivascular edema formation and disintegration of the structure; and grade 3 = dense neutrophil leukocyte infiltration and destruction of pulmonary structure (16).…”

Melatonin and 1400 W Ameliorate both Intestinal and Remote Organ Injury Following Mesenteric Ischemia/Reperfusion

“…Pulmonary injury was graded into four grades as follows: grade 0, no diagnostic change: grade 1, mild neutrophil leukocyte infiltration and mild to moderate interstitial congestion; grade 2, moderate neutrophil leukocyte infiltration, perivascular edema formation, and partial destruction of pulmonary architecture; and grade 3, included dense neutrophil leukocyte infiltration and complete destruction of pulmonary structure [40].…”

Increased poly(ADP-ribose) polymerase (PARP)-1 expression and activity are associated with inflammation but not goblet cell metaplasia in murine models of allergen-induced airway inflammation

“…Increased PARP-1 activity has also been shown to occur with lung inflammation triggered by acute respiratory distress syndrome [20], hyperoxic lung injury [21], distant (i.e., limb) tissue injury [18,19], as well as the allergic reaction seen in the murine OVA sensitization and challenge model of asthma studied here [43]. The responses of cells and tissues in such in vivo models are many and diverse, including inflammatory cell infiltration, the secretion of a multitude of cytokines, changes in redox state, and cellular responses ranging from cell death to cell replication and differentiation.…”

“…ROS are potent inducers of breaks in DNA [12][13][14], which in turn activate poly(ADP-ribose) polymerase-1 (PARP-1) [15], which then ADP-ribosylates histones, transcription factors, and PARP-1 itself [16,17], thus promoting an inflammatory response. A pathophysiological role for PARP-1 has been demonstrated in a number of pulmonary inflammatory disease models [18][19][20][21], as well as in other inflammatory models [18,20,[22][23][24]. It is also involved in nonpathologic processes such as DNA repair [25] and replication [26,27], cell cycle regulation and cell proliferation [28,29], differentiation [30,31], cell death [32,33], and mammalian development [22,[34][35][36].…”