OBJECTIVE:To investigate the efficacy of the Danlou Fang(DL)Traditional Chinese Medicine formula on microvascular obstruction(no-reflow)through the endothelial/inducible nitric oxide synthase(eNOS/iNOS)pathway in a ra...OBJECTIVE:To investigate the efficacy of the Danlou Fang(DL)Traditional Chinese Medicine formula on microvascular obstruction(no-reflow)through the endothelial/inducible nitric oxide synthase(eNOS/iNOS)pathway in a rat model.METHODS:Sprague-Dawley rats were subjected to 60 min of coronary artery occlusion(or sham procedure)followed by 2 h of reperfusion and were then divided into treatment groups:sham,model,DL(500 mg/kg),DL(500 mg/kg)+eNOS inhibitor L-nitroarginine(L-NNA;7.5 mg/kg),and sodium nitroprusside(SNP;0.5 mg/kg).There were 16 per group.Areas of no-reflow were determined by thioflavin S staining of heart tissue.Cardiac function was assessed by echocardiography.Myocardial enzymes and antioxidants in serum were measured and analyzed.The relative protein expression levels of eNOS and iNOS were determined by western blotting.RESULTS:DL had a myocardial protective effect on myocardial reperfusion and reduced the area of no-reflow.The serum levels of creatine kinase(CK),myocardial CK isoenzyme CK-MB,and lactate dehydrogenase were significantly lower in the DL group than in the model(P<0.05).DL treatment also decreased the serum content of malondialdehyde and reactive oxygen species(ROS),increased the activity of superoxide dismutase and nitric oxide,and promoted eNOS expression(P<0.05)while lowering iNOS expression.CONCLUSION:DL reduced the area of no-reflow and had a myocardial protective effect that may be associated with the eNOS/iNOS pathway.展开更多
AIM: To determine the expression of PGH synthase-1and the sensitivity of vascular smooth muscle to PGH_2in the aorta from the SHR at an age when noendothelium-dependent contractions to acetylcholine areobserved under ...AIM: To determine the expression of PGH synthase-1and the sensitivity of vascular smooth muscle to PGH_2in the aorta from the SHR at an age when noendothelium-dependent contractions to acetylcholine areobserved under control conditions. METHODS: Allexperiments were performed in parallel on aortas from20-wk-old SHR and Wistar-Kyoto normotensive rats(WKY). Rings, with or without endothelium, weresuspended in conventional organ chambers for therecording of changes in isometric force. Theexpression of PGH Synthase-1 was evaluated by展开更多
AIM: To study the effects of aminoguanidine (AG) and two L-arginine analogues N(omega)-nitro-L-arginine methyl ester (L-NAME) and N(omega)-nitro-L-arginine (L-NNA) on nitric oxide (NO) production induced by cytokines ...AIM: To study the effects of aminoguanidine (AG) and two L-arginine analogues N(omega)-nitro-L-arginine methyl ester (L-NAME) and N(omega)-nitro-L-arginine (L-NNA) on nitric oxide (NO) production induced by cytokines (TNF-alpha, IL-1 beta, and IFN-gamma) and bacterial lipopolysaccharide (LPS) mixture (CM) in the cultured rat hepatocytes, and examine their mechanisms action. METHODS: Rat hepatocytes were incubated with AG, L-NAME, L-NNA, Actinomycin D (ActD) and dexamethasone in a medium containing CM (LPS plus TNF-alpha, IL-1 beta, and IFN-gamma) for 24h. NO production in the cultured supernatant was measured with the Griess reaction. Intracellular cGMP level was detected with radioimmunoassy. RESULTS: NO production was markedly blocked by AG and L-NAME in a dose-dependent manner under inflammatory stimuli condition triggered by CM in vitro. The rate of the maximum inhibitory effects of L-NAME (38.9%) was less potent than that obtained with AG(53.7%, P 【 0.05). There was no significant difference between the inhibitory effects of AG and two L-arginine analogues on intracellular cGMP accumulation in rat cultured hepatocytes. Non-specific NOS expression inhibitor dexamethasone (DEX)and iNOS mRNA transcriptional inhibitor ActD also significantly inhibited CM-induced NO production. AG(0.1 mmol x L(-1)) and ActD (0.2 ng x L(-1)) were equipotent in decreasing NO production induced by inflammatory stimuli in vitro, and both effects were more potent than that induced by non-selectivity NOS activity inhibitor L-NAME (0.1 mmol x L(-1)) under similar stimuli conditions (P【0.01). CONCLUSION: AG is a potent selective inhibitor of inducible isoform of NOS,and the mechanism of action may be not only competitive inhibition in the substrate level, but also the gene expression level in rat hepatocytes.展开更多
AIM: To investigate the effect of L-NAME on nitric oxide and gastrointestinal motility alterations in cirrhotic rats. METHODS: Rats with cirrhosis induced by carbon tetrachloride were randomly divided into two groups,...AIM: To investigate the effect of L-NAME on nitric oxide and gastrointestinal motility alterations in cirrhotic rats. METHODS: Rats with cirrhosis induced by carbon tetrachloride were randomly divided into two groups, one n =13 receiving 0.5mg.kg(-1) per day of N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, for 10 days, whereas the other group (n =13) and control (n =10) rats were administrated the same volume of 9g.L(-1) saline. Half gastric emptying time and 2h residual rate were measured by SPECT, using (99m)Tc-DTPA-labeled barium sulfate as test meal. Gastrointestinal transition time was recorded simultaneously. Serum concentration of nitric oxide (NO) was determined by the kinetic cadmium reduction and colorimetric methods. Immunohistochemical SABC method was used to observe the expression and distribution of three types of nitric oxide synthase (NOS) isoforms in the rat gastrointestinal tract. Western blot was used to detect expression of gastrointestinal NOS isoforms. RESULTS: Half gastric emptying time and trans-gastrointestinal time were significantly prolonged(124.0 +/- 26.4 min; 33.7 +/- 8.9 min; 72.1 +/- 15.3 min; P【0.01), (12.4 +/- 0.5h; 9.5 +/- 0.3h; 8.2 +/- 0.8h; P【0.01), 2h residual rate was raised in cirrhotic rats than in controls and cirrhotic rats treated with L-NAME (54.9 +/- 7.6%,13.7 +/- 3.2%, 34.9 +/- 10.3%, P【0.01). Serum concentration of NO was significantly increased in cirrhotic rats than in the other groups (8.20 +/- 2.48) micromol.L(-1), (5.94 +/-1.07) micromol.L(-1) and control (5.66 +/- 1.60 micromol.L(-1), P【0.01. NOS staining intensities which were mainly located in the gastrointestinal tissues were markedly lower in cirrhotic rats than in the controls and cirrhotic rats after treated with L-NAME. CONCLUSION: Gastrointestinal motility was remarkably inhibited in cirrhotic rats, which could be alleviated by L-NAME. Nitric oxide may play an important role in the inhibition of gastrointestinal motility in cirrhotic rats.展开更多
Background Preeclampsia （PE） is a multifactorial pregnancy complication.Maternal underlying condition and adverse factors both influence the pathogenesis of PE.Abnormal lipid metabolism as a maternal underlying dise...Background Preeclampsia （PE） is a multifactorial pregnancy complication.Maternal underlying condition and adverse factors both influence the pathogenesis of PE.Abnormal lipid metabolism as a maternal underlying disease may participate in the occurrence and development of PE.This study aimed to observe the effects of adverse factors on PE-like symptoms of pregnant mice with genetic abnormal lipid metabolism.Methods Apolipoprotein C-Ⅲ （ApoC3） transgenic mice with abnormal lipid metabolism were subcutaneously injected with L-arginine methyl ester （L-NAME） or normal saline （NS） daily starting at Day 7 or 16 of pregnancy （ApoC3＋L-NA and ApoC3＋NS groups）,and wild-type （WT） mice served as a control （WT＋L-NA and WT＋NS groups）.All mice were subdivided into early and late subgroups by injection time.The mean arterial pressure （MAP） and urinary protein were measured.Pregnancy outcomes,including fetal weight,placental weight,live birth rate,and fetal absorption rate,were analyzed.Pathologic changes in the placenta were observed by hematoxylin-eosin staining.One-way analysis of variance,t-test,and x2 test were used for statistical analysis.Results MAP significantly increased for ApoC3＋NS groups compared with WT＋NS groups （P 〈0.05）,without significant difference in urine protein.Following L-NAME injection,MAP and urinary protein significantly increased for ApoC3＋L-NA and WT＋L-NA compared with the corresponding NS groups （P 〈0.05）,and the increase for ApoC3＋L-NA was more obvious.Urinary protein levels in early ApoC3＋L-NA and WT＋L-NA significantly increased compared with the corresponding late groups （P 〈0.05）.Fetal absorption rate significantly increased and fetal and placental weights significantly decreased in early ApoC3＋L-NA and WT＋L-NA compared with the corresponding NS groups （P 〈0.05）,without significant difference in late ApoC3＋L-NA and WT＋L-NA groups.Fetal weight in early ApoC3＋L-NA was significantly lower than in early WT＋L-NA 展开更多
AIML To investigate the effect and mechanism of action of the nitric oxide synthase （NOS） inhibitor NG-nitro-L-arginine methyl ester （L-NAME） on invasion and metastasis of human colorectal cancer cell line SL-174T...AIML To investigate the effect and mechanism of action of the nitric oxide synthase （NOS） inhibitor NG-nitro-L-arginine methyl ester （L-NAME） on invasion and metastasis of human colorectal cancer cell line SL-174T. METHODS： Human colorectal cancer cel4 line SL-174T was cultured and treated separately with four different dosages of L-NAME for 72 h, Nitric oxide （NO） production was measured with Griess reagent, The effect of L-NAME on invasion and migration of SL-174T cells were evaluated by using Transwell chambers attached with polycarbonate filters and reconstituted basement membrane （Matrigel）, RT-PCR was performed to determine the mRNA levels of matrix metalloproteinase-2 （MMP-2） and tissue inhibitor metalloproteinase-2 （TIMP-2）,RESULTS： L-NAME could significantly inhibit NO production of SL-174T in a dose-dependent manner. After being treated for 72 h with 0.2, 0.4, 0.8, and 1.0 mmol/L L- NAME, respectively, the ability of the L-NAME treated SL- 174T cells to invade the reconstituted basement membrane decreased significantly （t = 8.056, P〈0.05; t= 14.467, P〈0.01; t= 27.785, P〈0.01; and t= 29.405, P〈0.01, respectively） and the inhibition rates were 10.29%, 19.62%, 34.08%, and 42.23%, respectively. Moreover, L-NAME could inhibit migration of SL-174T cells, and the inhibition rates were 20.76%, 24.95%, 39.43%, and 46. 85% for L-NAME at 0.2, 0.4, 0.8, and 1.0 mmol/L, respectively （t = 15.116, P〈0.01）. In addition, after treatment with L-NAME, expression of MMP-2 mRNA was significantly decreased （t = 71.238, P〈0.01） and that of TIMP-2 mRNA was markedly increased （t = -13.020, P〈0.01）. CONCLUSION： L-NAME exerts anti-invasive and anti- metastatic effects on SL-174T cell line via downregulating MNP-2 mRNA expression and upregulating TIMP-2 mRNA expression.展开更多
BACKGROUND Although the associating liver partition and portal vein ligation for staged hepatectomy(ALPPS)induces more rapid liver regeneration than portal vein embolization,the mechanism remains unclear.AIM To assess...BACKGROUND Although the associating liver partition and portal vein ligation for staged hepatectomy(ALPPS)induces more rapid liver regeneration than portal vein embolization,the mechanism remains unclear.AIM To assess the influence of inflammatory cytokines and endothelial nitric oxide synthase(eNOS)activation on liver regeneration in ALPPS.METHODS The future liver remnant/body weight(FLR/BW)ratio,hepatocyte proliferation,inflammatory cytokine expression,and activation of the Akt-eNOS pathway were evaluated in rat ALPPS and portal vein ligation(PVL)models.Hepatocyte proliferation was assessed based on Ki-67 expression,which was confirmed using immunohistochemistry.The serum concentrations of inflammatory cytokines were measured using enzyme linked immune-solvent assays.The Akt-eNOS pathway was assessed using western blotting.To explore the role of inflammatory cytokines and NO,Kupffer cell inhibitor gadolinium chloride(GdCl3),NOS inhibitor N-nitro-arginine methyl ester(L-NAME),and NO enhancer molsidomine were administered intraperitoneally.RESULTS The ALPPS group showed significant FLR regeneration(FLR/BW:1.60%±0.08%,P<0.05)compared with that observed in the PVL group(1.33%±0.11%)48 h after surgery.In the ALPPS group,serum interleukin-6 expression was suppressed using GdCl3 to the same extent as that in the PVL group.However,the FLR/BW ratio and Ki-67 labeling index were significantly higher in the ALPPS group administered GdCl3(1.72%±0.19%,P<0.05;22.25%±1.30%,P<0.05)than in the PVL group(1.33%±0.11%and 12.78%±1.55%,respectively).Phospho-Akt Ser473 and phospho-eNOS Ser1177 levels were enhanced in the ALPPS group compared with those in the PVL group.There was no difference between the ALPPS group treated with L-NAME and the PVL group in the FLR/BW ratio and Ki-67 labeling index.In the PVL group treated with molsidomine,the FLR/BW ratio and Ki-67 labeling index increased to the same level as in the ALPPS group.CONCLUSION Early induction of inflammatory cytokines may not be pivotal for accelerated FLR regenera展开更多
文摘OBJECTIVE:To investigate the efficacy of the Danlou Fang(DL)Traditional Chinese Medicine formula on microvascular obstruction(no-reflow)through the endothelial/inducible nitric oxide synthase(eNOS/iNOS)pathway in a rat model.METHODS:Sprague-Dawley rats were subjected to 60 min of coronary artery occlusion(or sham procedure)followed by 2 h of reperfusion and were then divided into treatment groups:sham,model,DL(500 mg/kg),DL(500 mg/kg)+eNOS inhibitor L-nitroarginine(L-NNA;7.5 mg/kg),and sodium nitroprusside(SNP;0.5 mg/kg).There were 16 per group.Areas of no-reflow were determined by thioflavin S staining of heart tissue.Cardiac function was assessed by echocardiography.Myocardial enzymes and antioxidants in serum were measured and analyzed.The relative protein expression levels of eNOS and iNOS were determined by western blotting.RESULTS:DL had a myocardial protective effect on myocardial reperfusion and reduced the area of no-reflow.The serum levels of creatine kinase(CK),myocardial CK isoenzyme CK-MB,and lactate dehydrogenase were significantly lower in the DL group than in the model(P<0.05).DL treatment also decreased the serum content of malondialdehyde and reactive oxygen species(ROS),increased the activity of superoxide dismutase and nitric oxide,and promoted eNOS expression(P<0.05)while lowering iNOS expression.CONCLUSION:DL reduced the area of no-reflow and had a myocardial protective effect that may be associated with the eNOS/iNOS pathway.
文摘AIM: To determine the expression of PGH synthase-1and the sensitivity of vascular smooth muscle to PGH_2in the aorta from the SHR at an age when noendothelium-dependent contractions to acetylcholine areobserved under control conditions. METHODS: Allexperiments were performed in parallel on aortas from20-wk-old SHR and Wistar-Kyoto normotensive rats(WKY). Rings, with or without endothelium, weresuspended in conventional organ chambers for therecording of changes in isometric force. Theexpression of PGH Synthase-1 was evaluated by
基金Project supported by the National Natural Science Foundation of China,No.39770861.and JANSSEN Science Research Foundation.
文摘AIM: To study the effects of aminoguanidine (AG) and two L-arginine analogues N(omega)-nitro-L-arginine methyl ester (L-NAME) and N(omega)-nitro-L-arginine (L-NNA) on nitric oxide (NO) production induced by cytokines (TNF-alpha, IL-1 beta, and IFN-gamma) and bacterial lipopolysaccharide (LPS) mixture (CM) in the cultured rat hepatocytes, and examine their mechanisms action. METHODS: Rat hepatocytes were incubated with AG, L-NAME, L-NNA, Actinomycin D (ActD) and dexamethasone in a medium containing CM (LPS plus TNF-alpha, IL-1 beta, and IFN-gamma) for 24h. NO production in the cultured supernatant was measured with the Griess reaction. Intracellular cGMP level was detected with radioimmunoassy. RESULTS: NO production was markedly blocked by AG and L-NAME in a dose-dependent manner under inflammatory stimuli condition triggered by CM in vitro. The rate of the maximum inhibitory effects of L-NAME (38.9%) was less potent than that obtained with AG(53.7%, P 【 0.05). There was no significant difference between the inhibitory effects of AG and two L-arginine analogues on intracellular cGMP accumulation in rat cultured hepatocytes. Non-specific NOS expression inhibitor dexamethasone (DEX)and iNOS mRNA transcriptional inhibitor ActD also significantly inhibited CM-induced NO production. AG(0.1 mmol x L(-1)) and ActD (0.2 ng x L(-1)) were equipotent in decreasing NO production induced by inflammatory stimuli in vitro, and both effects were more potent than that induced by non-selectivity NOS activity inhibitor L-NAME (0.1 mmol x L(-1)) under similar stimuli conditions (P【0.01). CONCLUSION: AG is a potent selective inhibitor of inducible isoform of NOS,and the mechanism of action may be not only competitive inhibition in the substrate level, but also the gene expression level in rat hepatocytes.
基金National Natural Science Foundation of China,No.39970901
文摘AIM: To investigate the effect of L-NAME on nitric oxide and gastrointestinal motility alterations in cirrhotic rats. METHODS: Rats with cirrhosis induced by carbon tetrachloride were randomly divided into two groups, one n =13 receiving 0.5mg.kg(-1) per day of N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, for 10 days, whereas the other group (n =13) and control (n =10) rats were administrated the same volume of 9g.L(-1) saline. Half gastric emptying time and 2h residual rate were measured by SPECT, using (99m)Tc-DTPA-labeled barium sulfate as test meal. Gastrointestinal transition time was recorded simultaneously. Serum concentration of nitric oxide (NO) was determined by the kinetic cadmium reduction and colorimetric methods. Immunohistochemical SABC method was used to observe the expression and distribution of three types of nitric oxide synthase (NOS) isoforms in the rat gastrointestinal tract. Western blot was used to detect expression of gastrointestinal NOS isoforms. RESULTS: Half gastric emptying time and trans-gastrointestinal time were significantly prolonged(124.0 +/- 26.4 min; 33.7 +/- 8.9 min; 72.1 +/- 15.3 min; P【0.01), (12.4 +/- 0.5h; 9.5 +/- 0.3h; 8.2 +/- 0.8h; P【0.01), 2h residual rate was raised in cirrhotic rats than in controls and cirrhotic rats treated with L-NAME (54.9 +/- 7.6%,13.7 +/- 3.2%, 34.9 +/- 10.3%, P【0.01). Serum concentration of NO was significantly increased in cirrhotic rats than in the other groups (8.20 +/- 2.48) micromol.L(-1), (5.94 +/-1.07) micromol.L(-1) and control (5.66 +/- 1.60 micromol.L(-1), P【0.01. NOS staining intensities which were mainly located in the gastrointestinal tissues were markedly lower in cirrhotic rats than in the controls and cirrhotic rats after treated with L-NAME. CONCLUSION: Gastrointestinal motility was remarkably inhibited in cirrhotic rats, which could be alleviated by L-NAME. Nitric oxide may play an important role in the inhibition of gastrointestinal motility in cirrhotic rats.
基金his work was supported by a grant from the National Natural Science Foundation of China （No. 81370723） and the Specialized Research Fund for the Doctoral Program of Higher Education from the Ministry of Education of China （No. 20130001110111）.
文摘Background Preeclampsia （PE） is a multifactorial pregnancy complication.Maternal underlying condition and adverse factors both influence the pathogenesis of PE.Abnormal lipid metabolism as a maternal underlying disease may participate in the occurrence and development of PE.This study aimed to observe the effects of adverse factors on PE-like symptoms of pregnant mice with genetic abnormal lipid metabolism.Methods Apolipoprotein C-Ⅲ （ApoC3） transgenic mice with abnormal lipid metabolism were subcutaneously injected with L-arginine methyl ester （L-NAME） or normal saline （NS） daily starting at Day 7 or 16 of pregnancy （ApoC3＋L-NA and ApoC3＋NS groups）,and wild-type （WT） mice served as a control （WT＋L-NA and WT＋NS groups）.All mice were subdivided into early and late subgroups by injection time.The mean arterial pressure （MAP） and urinary protein were measured.Pregnancy outcomes,including fetal weight,placental weight,live birth rate,and fetal absorption rate,were analyzed.Pathologic changes in the placenta were observed by hematoxylin-eosin staining.One-way analysis of variance,t-test,and x2 test were used for statistical analysis.Results MAP significantly increased for ApoC3＋NS groups compared with WT＋NS groups （P 〈0.05）,without significant difference in urine protein.Following L-NAME injection,MAP and urinary protein significantly increased for ApoC3＋L-NA and WT＋L-NA compared with the corresponding NS groups （P 〈0.05）,and the increase for ApoC3＋L-NA was more obvious.Urinary protein levels in early ApoC3＋L-NA and WT＋L-NA significantly increased compared with the corresponding late groups （P 〈0.05）.Fetal absorption rate significantly increased and fetal and placental weights significantly decreased in early ApoC3＋L-NA and WT＋L-NA compared with the corresponding NS groups （P 〈0.05）,without significant difference in late ApoC3＋L-NA and WT＋L-NA groups.Fetal weight in early ApoC3＋L-NA was significantly lower than in early WT＋L-NA
文摘AIML To investigate the effect and mechanism of action of the nitric oxide synthase （NOS） inhibitor NG-nitro-L-arginine methyl ester （L-NAME） on invasion and metastasis of human colorectal cancer cell line SL-174T. METHODS： Human colorectal cancer cel4 line SL-174T was cultured and treated separately with four different dosages of L-NAME for 72 h, Nitric oxide （NO） production was measured with Griess reagent, The effect of L-NAME on invasion and migration of SL-174T cells were evaluated by using Transwell chambers attached with polycarbonate filters and reconstituted basement membrane （Matrigel）, RT-PCR was performed to determine the mRNA levels of matrix metalloproteinase-2 （MMP-2） and tissue inhibitor metalloproteinase-2 （TIMP-2）,RESULTS： L-NAME could significantly inhibit NO production of SL-174T in a dose-dependent manner. After being treated for 72 h with 0.2, 0.4, 0.8, and 1.0 mmol/L L- NAME, respectively, the ability of the L-NAME treated SL- 174T cells to invade the reconstituted basement membrane decreased significantly （t = 8.056, P〈0.05; t= 14.467, P〈0.01; t= 27.785, P〈0.01; and t= 29.405, P〈0.01, respectively） and the inhibition rates were 10.29%, 19.62%, 34.08%, and 42.23%, respectively. Moreover, L-NAME could inhibit migration of SL-174T cells, and the inhibition rates were 20.76%, 24.95%, 39.43%, and 46. 85% for L-NAME at 0.2, 0.4, 0.8, and 1.0 mmol/L, respectively （t = 15.116, P〈0.01）. In addition, after treatment with L-NAME, expression of MMP-2 mRNA was significantly decreased （t = 71.238, P〈0.01） and that of TIMP-2 mRNA was markedly increased （t = -13.020, P〈0.01）. CONCLUSION： L-NAME exerts anti-invasive and anti- metastatic effects on SL-174T cell line via downregulating MNP-2 mRNA expression and upregulating TIMP-2 mRNA expression.
文摘BACKGROUND Although the associating liver partition and portal vein ligation for staged hepatectomy(ALPPS)induces more rapid liver regeneration than portal vein embolization,the mechanism remains unclear.AIM To assess the influence of inflammatory cytokines and endothelial nitric oxide synthase(eNOS)activation on liver regeneration in ALPPS.METHODS The future liver remnant/body weight(FLR/BW)ratio,hepatocyte proliferation,inflammatory cytokine expression,and activation of the Akt-eNOS pathway were evaluated in rat ALPPS and portal vein ligation(PVL)models.Hepatocyte proliferation was assessed based on Ki-67 expression,which was confirmed using immunohistochemistry.The serum concentrations of inflammatory cytokines were measured using enzyme linked immune-solvent assays.The Akt-eNOS pathway was assessed using western blotting.To explore the role of inflammatory cytokines and NO,Kupffer cell inhibitor gadolinium chloride(GdCl3),NOS inhibitor N-nitro-arginine methyl ester(L-NAME),and NO enhancer molsidomine were administered intraperitoneally.RESULTS The ALPPS group showed significant FLR regeneration(FLR/BW:1.60%±0.08%,P<0.05)compared with that observed in the PVL group(1.33%±0.11%)48 h after surgery.In the ALPPS group,serum interleukin-6 expression was suppressed using GdCl3 to the same extent as that in the PVL group.However,the FLR/BW ratio and Ki-67 labeling index were significantly higher in the ALPPS group administered GdCl3(1.72%±0.19%,P<0.05;22.25%±1.30%,P<0.05)than in the PVL group(1.33%±0.11%and 12.78%±1.55%,respectively).Phospho-Akt Ser473 and phospho-eNOS Ser1177 levels were enhanced in the ALPPS group compared with those in the PVL group.There was no difference between the ALPPS group treated with L-NAME and the PVL group in the FLR/BW ratio and Ki-67 labeling index.In the PVL group treated with molsidomine,the FLR/BW ratio and Ki-67 labeling index increased to the same level as in the ALPPS group.CONCLUSION Early induction of inflammatory cytokines may not be pivotal for accelerated FLR regenera
