Anti-inflammatory effect of thalidomide in paraquat-induced pulmonary injury in mice

The effect of thalidomide on ethanol-induced gastric mucosal damage in mice: Involvement of inflammatory cytokines and nitric oxide

“…It is well known that iNOS activity and subsequent NO pro-371 duction can be induced by proinflammatory cytokines such as 372 TNF-a and IL-1b. In our previous studies, we showed that thalido-373 mide was able to prevent excessive production of NO by inhibition 374 of proinflammatory cytokines[18,19]. In the present study, our375 findings showed that ethanol exposure increased the levels of 376 nitrate as an index of NO formation in the gastric tissue.…”

“…# P < 0.001 compared with normal group; ⁄ P = 0.01 and ⁄⁄ P < 0.001 compared with ethanol control group. HOCl), which is toxic to cells[17,18]. In the present study,298 MPO activity was significantly increased in the gastric tissue fol-299 lowing ethanol administration and pretreatment with thalidomide 300 significantly reduced MPO activity in the animals receiving etha-301 nol.…”

“…It has been shown that neutrophil 60 infiltration into the gastric mucosa has a critical role in the devel- suppress the production of TNF-a, IL-1b, IL-6 and NO in gastroin-89 testinal tissue [13][14][15][16]. In addition, our previous studies have also 90 confirmed that thalidomide exerts its anti-inflammatory effects by 91 suppressing the production of proinflammatory cytokines [17][18][19]. 92 TNF-a has a major role in the pathophysiology of ethanol-induced 93 gastric mucosal inflammation and damage [7,9,20].…”

Protective effects of intranasal curcumin on paraquot induced acute lung injury (ALI) in mice

“…During respiratory burst, neutrophils produce hypochlorous acid (HOCL) involved in tissue damage during inflammation and oxidative stress. Several studies suggest that MPO level is higher in PQ induced inflammation and oxidative stress mediated lung injury (Amirshahrokhi, 2013;Tian et al, 2013). Intranasal curcumin pretreatment has significantly ameliorated enhanced MPO activity up to 50% after PQ intoxication.…”

Atorvastatin protected from paraquat-induced cytotoxicity in alveolar macrophages via down-regulation of TLR-4

“…Additionally it's cytotoxicity against functional and defender cells including macrophages has been documented. Pulmonary inflammation and fibrosis are the most common injuries produced by PQ poisoning (Amirshahrokhi, 2013;Xie et al, 2012). The main mechanism of PQ's toxicity is redox reaction by reactive oxygen species and lipid peroxidation of cellular membrane is a significant pathway.…”