Inflammation
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Laparoscopic surgery is performed by carbon dioxide (CO2) insufflation, but this may induce stress responses. The aim of this study is to compare the level of inflammatory mediators in patients receiving low tidal volume (VT) versus traditional VT during gynecological laparoscopic surgery. Forty American Society of Anesthesiologists (ASA) physical status 1 and 2 subjects older than 18 years old undergoing laparoscopic gynecological surgery were included. ⋯ An increase in the serum levels of IL-6, TNF-alpha, IL-8, and IL-1β was observed in both groups during the time periods of T1, T2, and T3. No significant differences were found in the serum and BAL levels of inflammatory mediators during time periods between groups. The results of the present study suggested that the lung-protective ventilation and traditional strategies are not different in terms of lung injury and inflammatory response during conventional laparoscopic gynecological surgery.
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We aimed to investigate the preventive and therapeutic effect of apocynin (APO) on bleomycin (BLC)-induced lung injury in rats. Rats were assigned into groups as follows: control group; APO group, 20 mg/kg APO was given intraperitoneal for 29 days; BLC-1 and BLC-2 groups, a single intratracheal injection of BLC (2.5 mg/kg); APO+BLC-preventive group, 20 mg/kg APO was administered 12 h before the intratracheal BLC injection and continued for 14 days; BLC+APO-treatment group, 20 mg/kg APO was given on the 14th day after the intratracheal BLC injection and continued to sacrifice. The BLC-1 group was sacrificed on the 14th day of BLC administration to validate BLC-induced lung inflammation and fibrosis on the 14th of study initiation. ⋯ Otherwise, APO administration, both before and after BLC, reversed all biochemical markers and cytokine as well as histopathological changes induced by BLC. Interestingly, APO treatment reversed MPO activity in serum increased by BLC. In this study, both protective and therapeutic effects of APO against BLC-induced lung fibrosis were demonstrated for the first time.
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Acute lung injury (ALI) is characterized by alveolar injury and uncontrolled inflammation. Mechanisms underlying pathogenesis of ALI are unknown. Regulatory T cells (Tregs), either natural or induced, suppress a variety of physiological and pathological immune responses. ⋯ Since Tim-3 is a negative regulatory molecule and can modulate the function of Tregs, we evaluated Tim-3 level on Tregs and identified upregulation of the molecule in patients than that in controls. Moreover, compared to those who died during the study, patients who survived showed 1.7-fold higher level of Tim-3 on Tregs at the time of recruitment (P<0.001). These results suggest that Tregs could affect the prognosis of ALI probably due to the upregulation of Tim-3.
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The purpose of the present study is to evaluate the effect of emu oil on bioavailability of curcumin when co-administered and to evaluate the property that enhances the anti-inflammatory potential of curcumin. Oral bioavailability of curcumin in combination with emu oil was determined by measuring the plasma concentration of curcumin by HPLC. ⋯ The increased anti-inflammatory activity in combination therapy is due to enhanced bioavailability (5.2-fold compared to aqueous suspension) of curcumin by emu oil. Finally, it is concluded that the combination of emu oil with curcumin will be a promising approach for the treatment of arthritis.
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Remifentanil significantly represses cell immune responses and influences neutrophil migration through endothelial cell monolayers. The present study determines the beneficial effects of remifentanil and the mechanisms by which it attenuates lipopolysaccharide (LPS)-induced acute lung injury (ALI). Rats were intratracheally instilled with 2 mg/kg LPS to induce ALI. ⋯ Remifentanil also attenuated the concentrations of proinflammatory cytokines tumor necrosis factor alpha, interleukin-1β, and interleukin-6 in BALF, as well as effectively repressed the activation of nuclear factor-kappaB (NF-κB), which has been associated with the inhibition of IκBα degradation. These results suggest that remifentanil may be a suitable treatment for LPS-induced ALI. Remifentanil exerts beneficial effects on the inhibition of proinflammatory cytokine production by downregulating the NF-κB pathway.