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Objective To investigate the effects of breviscapine injection on intestinal injury induced by intestine ischemia-reperfusion(IIR). Methods 48 males SD rats with 8-week old were randomly divided into 4 groups:Sham,intestine ischemia-reperfusion(IIR),EB+IIR,TP+IIR. Breviscapine injection 20 mg/(kg·d) was given intraperitoneally in EB + IIR group. TPCA-1(12 mg/kg)was given intravenously 30 min before surgery in TP+IIR group. Rats were subjected to superior mesenteric artery occlusion consisting of 45 min of ischemia and 6 h of reperfusion;sham laparotomy served as controls. Intestine pathology was assayed by H&E staining. Con-centrations of TNF-α,IL-1β,and IL-6 in intestinal mucosa were determined by ELISA. The protein expressions of IκB-α,NF-κB ,ICAM-1of intestine tissue were assayed by western blot. Results IIR induced serious intesti-nal injury ,evidenced as poor intestine pathology ,elevation of TNF-α,IL-1β,and IL-6 levels in intestinal mu- cosa,accompanied with IκB-α/NF-κB/ICAM-1 pathway activation. However,breviscapine injection pretreatment could inhibit IκB-α/NF-κB/ICAM-1 pathway activation,leading to reduction of TNF-α,IL-1β,and IL-6 concen-trations in lung,finally attenuate ALI induced by IIR. Conclusion Breviscapine injection pretreatment could atten-uate inflammation in intestine after IIR injury via inhibiting IκB-α/NF-κB/ICAM-1signaling pathway.
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Objective To investigate the effect and mechanism of epigallocatechin-3-gallate(EGCG) on intestine ischemia reperfusion injury(IRI) in rats. Methods Forty SD rats were randomly and equally divided into 4 groups:sham group(Sham),intestinal ischemia reperfusion injury group(IRI),EGCG pretreatment group(EGCG) and HLY78 group (Wnt-Ag).The IRI,EGCG and WNT-AG groups were performed the superior mesenteric artery(SMA) ligation for 45 min by non-injury vascular clamp to construct the IRI model.EGCG (50 mg/kg) was administrated by intraperitoneal injection at 45 min before ischemia in EGCG group.The Wnt-Ag group was administrated by intraperitoneal injection of EGCG(50 mg/kg) plus Wnt-Ag (5 mg/kg) at 45 min before ischemia.The IRI group and Sham group were administrated by same dosage of normal saline.The pathological morphology of intestinal tissue was observed by staining at 4 h after reperfusion.The cellular apoptosis was detected by immunohistochemistry.The expressions of tumor necrosis factor-α(TNF-α),interleukin-1(IL-1),interleukin-6(IL-6) in the serum and intestinal tract were examined by ELISA and RT-PCR.The expressions of Wnt,β-catenin,p53,Bax and BCL-2 were measured by Western blot.Results Compared with the Sham group,the expression of IL-6,IL-1,TNF-α,Wnt,β-catenin,Bax,cell apoptosis and pathological change of intestinal tract in the IRI group were significantly increased,while the expression of BCL-2 was significantly decreased.Compared with the IRI group,the expression of IL-6,IL-1,TNF-α,Wnt,β-catenin,p53,Bax,cell apoptosis and the pathological change of intestinal tracrt in the EGCG group were significantly decreased,while the expression of BCL-2 was significantly increased.Compared with the EGCG group,the expression of IL-6,IL-1,TNF-α,Wnt,β-catenin,Bax,cell apoptosis and pathological change of intestinal tract in the Wnt-Ag group were increased,while the expression of BCL-2 was significantly decreased.Conclusion EGCG can alleviate intestine ischemia-reperfusion injury by suppressing inflammation and apoptosis,this protective effect may be mediated by suppressing Wnt/β-catenin signal pathway.
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Objective To investigate the effects of breviscapine injection on intestinal mucosal barrier damage induced by intestine ischemia-reperfusion (IIR). Methods 44 old SD rats were randomly divided into four groups:sham,intestine ischemia-reperfusion(IIR),EB+IIR,LN+IIR. Breviscapine injection 20 mg/(kg·d) was given intraperitoneally in EB+IIR group. L-NAME(100 mg/kg)was given intravenously 30 min before surgery in LN+IIR group. Rats were subjected to superior mesenteric artery occlusion consisting of 45 min of ischemia and 4 h of reperfusion;sham laparotomy served as controls. Intestine pathology was assayed by H&E staining. Concen-trations of SIgA,iNOS,eNOS and NO in intestinal mucosa,also endotoxine in plasma,were determined by ELI-SA. Results IIR induced serious intestinal mechanical and immune barrier damage ,evidenced as poor intestine pathology,depression of intestinal SIgA and eNOS levels,elevation of intestinal iNOS/NO levels. However,brevis-capine injection pretreatment could promote eNOS/NO production ,down-regulated iNOS expression ,leading to ele-vating SIgA concentration in intestine ,attenuate endotoxemia induced by IIR. The protection was canceled when application of L-NAME. Conclusion Breviscapine pretreatment attenuates ischemia-reperfusion-induced intestinal mucosal barrier damage via promoting eNOS/NO production.
ABSTRACT
Objective To investigate the effects of breviscapine injection on intestinal injury induced by intestine ischemia-reperfusion(IIR). Methods 48 males SD rats with 8-week old were randomly divided into 4 groups:Sham,intestine ischemia-reperfusion(IIR),EB+IIR,TP+IIR. Breviscapine injection 20 mg/(kg·d) was given intraperitoneally in EB + IIR group. TPCA-1(12 mg/kg)was given intravenously 30 min before surgery in TP+IIR group. Rats were subjected to superior mesenteric artery occlusion consisting of 45 min of ischemia and 6 h of reperfusion;sham laparotomy served as controls. Intestine pathology was assayed by H&E staining. Con-centrations of TNF-α,IL-1β,and IL-6 in intestinal mucosa were determined by ELISA. The protein expressions of IκB-α,NF-κB ,ICAM-1of intestine tissue were assayed by western blot. Results IIR induced serious intesti-nal injury ,evidenced as poor intestine pathology ,elevation of TNF-α,IL-1β,and IL-6 levels in intestinal mu- cosa,accompanied with IκB-α/NF-κB/ICAM-1 pathway activation. However,breviscapine injection pretreatment could inhibit IκB-α/NF-κB/ICAM-1 pathway activation,leading to reduction of TNF-α,IL-1β,and IL-6 concen-trations in lung,finally attenuate ALI induced by IIR. Conclusion Breviscapine injection pretreatment could atten-uate inflammation in intestine after IIR injury via inhibiting IκB-α/NF-κB/ICAM-1signaling pathway.
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Objective This study aims to investigate the effect of Lipoxin A4 receptor on acute lung injury (ALI) induced by intestine ischemia-reperfusion (IIR). Methods Thirty-two 8-week old SD rats were randomly divided into four groups: sham, intestine ischemia-reperfusion (IIR), IIR + BML111 (BML-111), Boc-2 + IIR +BML111 (Boc-2). BML-111 (1 mg/kg) was given intraperitoneally at the onset of reperfusion in the BML-111 and the Boc-2 group. Boc-2 (50 μg/kg) was given intraperitoneally after anesthesia in the Boc-2 group. Rats were subjected to superior mesenteric artery occlusion consisting of 45-min ischemia and 6-h reperfusion, and the sham laparotomy was served as controls. The lung pathology was assayed by the H&E staining. Lung water content was detected using dry/wet ratio. Concentrations of TNF-α, IL-1β, and IL-6 in lung tissue were determined by ELISA. The protein expression of p38 MAPK and NF-κB of lung was assayed by western blot. Results IIR induced serious ALI, with poor lung pathology and increased lung water content, elevation of TNF-α, IL-1β, and IL-6 levels in lung, accompanied with activation of p38 MAPK/NF-κB pathway. However, BML-111 could inhibit the activation of p38 MAPK/NF-κB pathway, leading to the reductions of TNF-α, IL-1β, and IL-6 in lung and attenuation of IIR-induced ALI. Conclusion BML-111 treatment could attenuate inflammation in lung after IIR injury via inactivating the p38 MAPK/NF-κB signaling pathway.
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Objective To investigate the change of high mobility group box 1 ( HMGBI ) after intestine ischemia reperfusion (I/R) in rats, compare the effect of drainage of intestine lymph fluid on gut barrier, and ex- plore the possible mechanism of iachemia-reporfusion injury. Methods Thirty-two Sprague-Dawley (SD) rats (SPF grade) were randomly divided into4 groups with 8 rats in each group: blank group, sham group, intestine is-chemia-reperfusion (I/R) group, and intestine ischemia-reperfusion with drainage of intestine lymph fluid (I/R +drainage) group. Indicators of gut barrier function damage, translocation of endotoxin, and change of HMGB1 and cytokines were detected after intestine ischemia-reperfusion injury. Results The gut barrier function damage and levels of endotoxin, HMGBI, tumour necrosis factor-alpha ( TNF-α), interleukin-6 ( IL-6 ), interleukin-1 beta (IL-1β), and soluble intercellular adhesion molecule-1 (sICAM-1) were significantly lower in blank group and sham group than in I/R group and I/R + drainage group ( P < 0. 05 ). Compared with the intestine I/R + drainage group, the levels of endotoxin and cytokines were significantly higher in the intestine I/R group. The level of HMGB1 was slightly higher than that in the intestine I/R + drainage group, but such difference was not statistically significant ( P > 0. 05 ). lmmunohistochemical staining also revealed that the expression of HMGB1 was significant- ly higher in I/R group than in I/R + drainage group. Conclusions Intestine iachemia-reperfusion injury can lead to the injury of intestine mucosal barrier and increase HMGB1 level HMGB1 may deteriorate gut barrier function and increase the leveh of systemic cytokines. Drainage of lymph fluid can block the gut-lymph pathway and thus decrease the levels of endotoxin and cytokines in systemic circulation and attenuate intestine ischemia-reperfusion injury.