scholarly journals Resveratrol Reduces the Incidence of Portal Vein System Thrombosis after Splenectomy in a Rat Fibrosis Model

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Meng Xu ◽  
Wanli Xue ◽  
Zhenhua Ma ◽  
Jigang Bai ◽  
Shengli Wu
Keyword(s):  
Platelet Aggregation ◽  
Portal Vein ◽  
Low Molecular Weight ◽  
Sham Operation ◽  
Radical Oxygen Species ◽  
Vein System ◽  
Platelet Apoptosis ◽  
Sd Rats ◽  
Biochemical Assays ◽  
Underlying Mechanisms

Purpose. To investigate the preventive effect of resveratrol (RES) on the formation of portal vein system thrombosis (PVST) in a rat fibrosis model.Methods. A total of 64 male SD rats, weighing 200–300 g, were divided into five groups: Sham operation, Splenectomy I, Splenectomy II, RES, and low molecular weight heparin (LMWH), with the former two groups as nonfibrosis controls. Blood samples were subjected to biochemical assays. Platelet apoptosis was measured by flow cytometry. All rats were euthanized for PVST detection one week after operation.Results. No PVST occurred in nonfibrosis controls. Compared to Splenectomy II, the incidences of PVST in RES and LMWH groups were significantly decreased (bothp<0.05). Two rats in LMWH group died before euthanasia due to intra-abdominal hemorrhage. In RES group, significant decreases in platelet aggregation, platelet radical oxygen species (ROS) production, and increase in platelet nitric oxide (NO) synthesis and platelet apoptosis were observed when compared with Splenectomy II (allp<0.001), while in LMWH group only significant decrease in platelet aggregation was observed.Conclusion. Prophylactic application of RES could safely reduce the incidence of PVST after splenectomy in cirrhotic rat. Regulation of platelet function and induction of platelet apoptosis might be the underlying mechanisms.

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

2021 ◽  
Author(s):  
Fuli Ya ◽  
Kongyao Li ◽  
Hong Chen ◽  
Zezhong Tian ◽  
Die Fan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Protocatechuic Acid ◽  
Human Platelets ◽  
Ros Generation ◽  
Inhibitory Effects ◽  
Platelet Apoptosis ◽  
Phosphatidylserine Exposure ◽  
Underlying Mechanisms

AbstractOxidative stress plays crucial roles in initiating platelet apoptosis that facilitates the progression of cardiovascular diseases (CVDs). Protocatechuic acid (PCA), a major metabolite of anthocyanin cyanidin-3-O-β-glucoside (Cy-3-g), exerts cardioprotective effects. However, underlying mechanisms responsible for such effects remain unclear. Here, we investigate the effect of PCA on platelet apoptosis and the underlying mechanisms in vitro. Isolated human platelets were treated with hydrogen peroxide (H2O2) to induce apoptosis with or without pretreatment with PCA. We found that PCA dose-dependently inhibited H2O2-induced platelet apoptosis by decreasing the dissipation of mitochondrial membrane potential, activation of caspase-9 and caspase-3, and decreasing phosphatidylserine exposure. Additionally, the distributions of Bax, Bcl-xL, and cytochrome c mediated by H2O2 in the mitochondria and the cytosol were also modulated by PCA treatment. Moreover, the inhibitory effects of PCA on platelet caspase-3 cleavage and phosphatidylserine exposure were mainly mediated by downregulating PI3K/Akt/GSK3β signaling. Furthermore, PCA dose-dependently decreased reactive oxygen species (ROS) generation and the intracellular Ca2+ concentration in platelets in response to H2O2. N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3β signaling, caspase-3 activation, and phosphatidylserine exposure. The combination of NAC and PCA did not show significant additive inhibitory effects on PI3K/Akt/GSK3β signaling and platelet apoptosis. Thus, our results suggest that PCA protects platelets from oxidative stress-induced apoptosis through downregulating ROS-mediated PI3K/Akt/GSK3β signaling, which may be responsible for cardioprotective roles of PCA in CVDs.

Endothelium dependent expression and underlying mechanisms of des-Arg9-bradykinin-induced B1R-mediated vasoconstriction in rat portal vein

Peptides ◽  
2012 ◽  
Vol 37 (2) ◽  
pp. 216-224 ◽  
Author(s):  
Fernanda L. Basei ◽  
Daniela A. Cabrini ◽  
Cláudia P. Figueiredo ◽  
Stefânia Forner ◽  
Daniela B. Hara ◽  
...  
Keyword(s):  
Portal Vein ◽  
Rat Portal Vein ◽  
Underlying Mechanisms

scholarly journals The Effect of Low Molecular Weight Dextran on Serum Lipid and and Platelet Aggregation

1979 ◽  
Vol 7 (2) ◽  
pp. 315-324
Author(s):  
Fumio KUZUYA ◽  
Noboru YOSHIMINE ◽  
Katsunari FUZITA ◽  
Shoshi KATO ◽  
Nobuo SAKAMOTO
Keyword(s):  
Molecular Weight ◽  
Platelet Aggregation ◽  
Serum Lipid ◽  
Low Molecular Weight

Combined proteomic and metabonomic studies in three genetic forms of the renal Fanconi syndrome

2007 ◽  
Vol 293 (2) ◽  
pp. F456-F467 ◽  
Author(s):  
Annalisa Vilasi ◽  
Pedro R. Cutillas ◽  
Anthony D. Maher ◽  
Severine F. M. Zirah ◽  
Giovambattista Capasso ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Fanconi Syndrome ◽  
Low Molecular Weight ◽  
Renal Fanconi Syndrome ◽  
Dent’S Disease ◽  
H Nmr ◽  
Low Molecular Weight Proteinuria ◽  
Dent's Disease ◽  
Underlying Mechanisms ◽  
Normal Urine

The renal Fanconi syndrome is a defect of proximal tubular function causing aminoaciduria and low-molecular-weight proteinuria. Dent's disease and Lowe syndrome are defined X-linked forms of Fanconi syndrome; there is also an autosomal dominant idiopathic form (ADIF), phenotypically similar to Dent's disease though its gene defect is still unknown. To assess whether their respective gene products are ultimately involved in a common reabsorptive pathway for proteins and low-molecular-mass endogenous metabolites, we compared renal Fanconi urinary proteomes and metabonomes with normal (control) urine using mass spectrometry and1H-NMR spectroscopy, respectively. Urine from patients with low-molecular-weight proteinuria secondary to ifosfamide treatment (tubular proteinuria; TP) was also analyzed for comparison. All four of the disorders studied had characteristic proteomic and metabonomic profiles. Uromodulin was the most abundant protein in normal urine, whereas Fanconi urine was dominated by albumin.1H-NMR spectroscopic data showed differences in the metabolic profiles of Fanconi urine vs. normal urine, due mainly to aminoaciduria. There were differences in the urinary metabolite and protein compositions between the three genetic forms of Fanconi syndrome: cluster analysis grouped the Lowe and Dent's urinary proteomes and metabonomes together, whereas ADIF and TP clustered together separately. Our findings demonstrate a distinctive “polypeptide and metabolite fingerprint” that can characterize the renal Fanconi syndrome; they also suggest that more subtle and cause-specific differences may exist between the different forms of Fanconi syndrome that might provide novel insights into the underlying mechanisms and cellular pathways affected.

scholarly journals Low Molecular Weight Heparin in Portal Vein Thrombosis of Cirrhotic Patients: Only Therapeutic Purposes?

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Raffaele Licinio ◽  
Mariabeatrice Principi ◽  
Giuseppe Losurdo ◽  
Nicola Maurizio Castellaneta ◽  
Enzo Ierardi ◽  
...  
Keyword(s):  
Portal Vein ◽  
Portal Vein Thrombosis ◽  
High Rate ◽  
Low Molecular Weight ◽  
Vein Thrombosis ◽  
If Current ◽  
General Feeling ◽  
Cirrhotic Patients ◽  
Current Guidelines ◽  
Hepatic Synthesis

Cirrhosis has always been regarded as hemorrhagic coagulopathy caused by the reduction in the hepatic synthesis of procoagulant proteins. However, with the progression of liver disease, the cirrhotic patient undergoes a high rate of thrombotic phenomena in the portal venous system. Although the progression of liver failure produces a reduction in the synthesis of anticoagulant molecules, a test able to detect the patients with hemostatic balance shifting towards hypercoagulability has not yet been elaborated. The need of treatment and/or prophylaxis of cirrhotic patients is demonstrated by the increased mortality, the risk of bleeding from esophageal varices, and the mortality of liver transplantation, when portal vein thrombosis (PVT) occurs even if current guidelines do not give indications about PVT treatment in cirrhosis. In view of the general feeling that the majority of cirrhotic patients at an advanced stage may be in a procoagulant condition (suggested by the sharp increase in the prevalence of PVT), it is presumable that a prophylaxis of this population could be of benefit. The safety and the efficacy of prophylaxis and treatment with enoxaparin in patients with cirrhosis demonstrated by a single paper suggest this option only in controlled trials and, currently, there are no sufficient evidences for a recommendation in the clinical practice.

Hydroxychloroquine Blocks Autophagy and Promotes Apoptosis of the Prostate after Castration in Rats

2020 ◽  
Vol 104 (11-12) ◽  
pp. 968-974
Author(s):  
Sheng-Tao Ling ◽  
Chun-Lei Deng ◽  
Li Huang ◽  
Qi-Sheng Yao ◽  
Cui Liu ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Morphological Changes ◽  
Control Group ◽  
Sham Operation ◽  
Related Gene ◽  
Rt Pcr ◽  
Bax Protein ◽  
Sd Rats ◽  
Immunohistochemical Analyses ◽  
Scanning Electron

Autophagy is an important pro-survival mechanism and closely related to apoptosis. The aim of this study was to investigate whether hydroxychloroquine (HCQ) blocks autophagy and promotes apoptosis of the prostate after castration. <b><i>Methods:</i></b> Thirty-six male SD rats were randomly divided into 3 groups (<i>n</i> = 12): control group (sham operation), castration group, and HCQ group (castrated and treated with HCQ). On day 7, all mice were executed and prostates were isolated. The morphological changes of prostates were observed by light microscope, and the ultrastructure changes were observed under scanning electron microscope (SEM). The protein expression of Beclin-l, P62, caspase-3, Bcl-2, and Bax was assessed by immunohistochemical analyses. The mRNA expression of microtubule-associated protein light chain 3 (LC3) and autophagy-related gene 5 (Atg5) was detected by RT-PCR. <b><i>Results:</i></b> Prostates of castration group shrank remarkably and prostates of HCQ group shrank more remarkably than castration group. Cytolysosomes were visible in the prostates of the castration group under SEM. Immunohistochemistry showed that the protein of Beclin-1 increased in the castration group compared to the control group, while decreased in the HCQ group compared to the castration group. While P62 protein moderately dyed in the control group and weakly dyed in the castration group, it strongly dyed in the HCQ group. Caspase-3 and Bax protein were weakly dyed in the control group but moderately dyed in the castration group and strongly dyed in the HCQ group. The expressions of apoptosis suppressor Bcl-2 were reduced in the castration group and further reduced in the HCQ group compared to the castration group. RT-PCR revealed that the mRNA of LC3 and Atg5 in the castration group increased compared to the control group, while decreased after treated with HCQ. <b><i>Conclusion:</i></b> Autophagy increased after castrated in prostates, while decreased after treated with HCQ; all these indicated that HCQ blocked autophagy and then promoted prostate apoptosis of castrated mice.

Sign in / Sign up

Export Citation Format

Share Document