Effects of Prostaglandins and Leukotrienes on Hypoxic Pulmonary Vasoconstriction in Rats

To investigate the effects of prostaglandins (PGs) and leukotrienes (LTs) on hypoxic pulmonary vasoconstriction (HPV), in vivo rats experiment and in vitro perfused lung experiment were conducted. The effect of hypoxia on hemodynamics, concentrations of TXB 2 and 6 keto PGF 1α in serum and lung tissue during hypoxia and effects of PGs and LTs on HPV were observed. The results showed that pulmonary arterial pressure (P pa ) and pulmonary vascular resistance were increased during hypoxia, but cardiac output and systemic arterial pressure were decreased. There were increases of the concentrations of TXB 2 and 6 keto PGF 1α and their ratio in serum and lung tissue during hypoxia. After use of cyclooxygenase inhibitor (indomethacin) in vivo and in vitro , HPV was augmented respectively, but after use of lipoxygenase inhibitor (diethylcorbamazine) or leukotriene receptor blocker (LY 171883), HPV was attenuated. It was suggested that LTs mediated pulmonary vasoconstriction, PGs inhibited pulmonary vasoconstriction and they played a modulating role during hypoxia.

EFFECT OF CAPTOPRIL ON RENAL HEMODYNAMICS AND RENAL PROSTAGLANDINS IN EARLY TYPE Ⅱ DIABETIC PATIENTS WITH NORMO-OR MICROALBUMINURIA

In this study,we investigated the effect of captopril(CPT) on glomerular filtration rate(GFR),effective renal plasma flow(ERPF),filtration fraction(FF),urinary albumin excretion(UAE) and daily urinary excretion of thromboxane B2(TXB2) and 6-keto-prostaglandin F1a(6-keto-PGFla) in 29 normotensive non-insulin-dependent diabetes(NIDDM) patients without clinically discernible nephropathy.Before treatment,urinary excretion 6-keto-PGF1a was significantly increased(P<0.05) in 29 NIDDM patients compared with 25 health subjects matched for age and sex.The values of GFR and FF were significantly higher(P<0.01 and P<0.005,respectively) in NIDDM than in normal volunters,whereas ERPF was comparable in both groups.Meanwhile we observed that UAE of early NIDDM was increased before treatment.After CPT treatment,GFR,FF,UAE and urinary excretion of 6-keto-PGFla were significantly reduce(all P<0.005) compared with those of NIDDM before treatment. These data indicated that CPT is effective in lowering glomerular filtration pressure and ameliorating microalbuminuria in the normotensive early NIDDM.

Effects and Interactions of Prostaglandins and Interferon－γ on Steroidogenesis ofHuman Luteal Cells

Previous work from our laboratory has demonstrated that T lymphocyte-derived cytokine,interferon-gamma(IFN-γ) may play a role in human luteal regression by inhibiting luteal progesterone production.Prostaglandin F2αhas been known as an important luteolytic factor in a wide range of mammalian species.It was of interest to investigate the effects of IFN-γon prostaglandin synthesis and their possible interaction with the inhibition on human luteal steroidogenesis.Human luteal cells were cultured for four days in the presence or absence of IFN-γ.Simultaneously, the productions of progesterone,prostaglandin F2α(PGF2α),Prostaglandin E2(PGE2),and 6-ketoprostaglandin F1α(PGF1α) were evaluated.Concomitant with the inhibition of progesterone production induced by IFN-γ,αbiphasic pattern of response of prostaglandin synthesis was observed,i.e.a slight decrease of PGF2αand PGF1αafterα48 h exposure to IFN-γ while an increase of PGE2 after 96 h. In a separate experiment,a luteotropic action of PGE2 and PGF2a on human luteal cells from different stages was observed during 48 and 96 h periods of culture.In addition,while indomethacin(INDO) treatment markedly blocked the prostaglandin synthesis, the hasal as well as hCG stimulated progesterone production was still inhibited by IFN-γas usual.These results suggested that prostaglandins appeared to be not responsible for the observed inhibition Of progesterone production since the inhibitory effect was not influenced by concurrent treatment with INDO which suppressed prostaglandin synthesis.

A STUDY ON THE ALTERATION OF FREE RADICALS、PROSTAGLANDINS AND THEIR RELATIONSHIP IN CHILDREN EITH ACUTE GLOMERULONEPHRITIS

AGN and 34 healthy children were investigated in this study to research FRs and PGs roles in the patbyphysiology process with AGN.We measured the plasma levels of TXB2,6-KPGF1a,LPO, SOD,GSH-px,etc.by radioimmunoassay method.The result showed that,in acute phase of AGN,the level of LPO and TXB2 increased(P< 0. 01,P<0.001),but that of GSH-px and 6KPGF1a decreased(both P<0.001 )significantly. Meanwhile, there was a significant positive correlation between LPO and TXB2(r=0. 475,P<0.001 ), and a negative correlation between LPO and 6-KPGF1a(r=-0. 636,P<0. 001).All these indicate that FRs and PGs were all involved in the process of AGN and FRs destroyed renal tissue and physiology function themselves or by PGs generating.

Heparin-binding proteins from boar seminal plasma affecting the release of prostaglandins and interleukin-6 by porcine endometrial and cervical cells and bovine endometrial cells

The objectives of this study were to explore whether heparin-binding proteins, separated by fast protein liquid chromatography from boar seminal plasma influence the release of prostaglandins F2α, (PGF2α), E2 (PGE2) and interleukin-6 (IL-6) by porcine endometrial and cervical cells and even bovine endometrial cells. In Experiment I, we showed that release of PGF2α by endometrial epithelial, endometrial stromal and cervical stromal cells to the medium was inhibited (p α (TNFα) stimulated release of IL-6 by endometrial and cervical stromal cells after 24 h incubation, but in the presence of heparin-binding proteins, this stimulation was attenuated. Release of PGF2α by cryopreserved (Experiment II) and primary (Experiment III) cervical stromal cells was significantly inhibited after 3 h incubation with 66 - 95.4 μg of heparin- binding proteins. A significant inhibition of PGE2 release by cryopreserved and primary cervical stromal cells was already achieved after incubation with 16.5 - 23.9 μg of heparin-binding proteins. The release of IL-6 by cryopreserved cells was stimulated after 3 h incubation with heparin- binding proteins in a dose dependent manner in contrast to the release of IL-6 by freshly isolated cervical stromal cells. We also found (Experiment IV) that porcine heparin-binding seminal plasma proteins inhibited release of PGF2α and stimulated release of IL-6 by bovine endometrial epithelial cells. In conclusion, a group of heparin-binding proteins separated by fast protein liquid chromatography from boar seminal plasma inhibit PGF2α, PGE2 and stimulate IL-6 release by porcine endometrial and cervical cells and even by bovine endometrial cells. Thus, these proteins have a similar effect as the entire seminal plasma.

Relationship of cyclic stretching of human patellar tendon fibroblasts with abnormal increase of prostaglandins E2 and leukotriene B4

To investigate the relationship between tendinopathy and higher production of prostaglandins E2 (PGE2) and leukotriene B4(LTB4) induced by cyclic stretching of human patellar tendon fibroblasts.Methods We used a novel in vitro model system to mimic in vivo conditions,where human patellar tendon fibroblasts (HPTFs) were uniaxially stretched with different magnitudes of stretching (4%,8% and 12%).Non-stretched fibroblasts were used as control.The productions of PGE2 and LTB4 as well as the expression of cycloxygenase (COX) and 5-lipoxygenase (5-LO) were then measured every four hours of cyclic stretching.In addition,we treated the cells with inhibitors of COX or 5-LO.Results It was found that cyclic stretching of fibroblasts at 8% and 12% of stretching increased PGE2 and LTB4 levels.Blocking the COX enzyme with indomethacin (25 mol/L) decreased PGE2 levels but increased LTB4 production and vice versa.Whereas decreasing LTB4 production with MK-886 (10 μmol/L) could increase PGE2 levels compared to cells tretched without inhibitors.Conclusion Cyclic stretching of HPTFs produces high levels of PGE2 and LTB4,where a balance exists:blocking PGE2 production increases the production of LTB4,and vice versa.Therefore,this study raises the possibility that the routine use of COX inhibitors in clinical treatment of tendinopathy may exacerbate the condition by causing neutrophil-mediated inflammatory and degenerative changes in the tendon due to increased levels of LTB4,which is a potent chemoattractant for neutrophils.17 refs,3 figs.

Gastro-protective action of lafutidine mediated by capsaicin-sensitive afferent neurons without interaction with TRPV1 and involvement of endogenous prostaglandins

AIM： Lafutidine, a histamine H2 receptor antagonist, exhibits gastro-protective action mediated by capsaicinsensitive afferent neurons （CSN）. We compared the effect between lafutidine and capsaicin, with respect to the interaction with endogenous prostaglandins （PG）, nitric oxide （NO） and the afferent neurons, including transient receptor potential vanilloid subtype 1 （TRPV1）. METHODS： Male SD rats and C57BL/6 mice, both wildtype and prostacyclin IP receptor knockout animals, were used after 18 h of fasting. Gastric lesions were induced by the po administration of HCl/ethanol （60% in 150 mmol/L HCl） in a volume of 1 mL for rats or 0.3 mL for mice. RESULTS： Both lafutidine and capsaicin （1-10 mg/kg, po） afforded dose-dependent protection against HCI/ ethanol in rats and mice. The effects were attenuated by both the ablation of CSN and pretreatment with NG-nitro- L-arginine methyl ester, yet only the effect of capsaicin was mitigated by prior administration of capsazepine, the TRPV1 antagonist, as well as indomethacin. Lafutidine protected the stomach against HCl/ethanol in IP receptor knockout mice, similar to wild-type animals, while capsaicin failed to afford protection in the animals lacking IP receptors. Neither of these agents affected the mucosal PGE2 or 6-keto PGF1α contents in rat stomachs. Capsaicin evoked an increase in [Ca^2＋]i in rat TRPV1-transfected HEK293 cells while lafutidine did not. CONCLUSION： These results suggest that although both lafutidine and capsaicin exhibit gastro-protective action mediated by CSN, the mode of their effects differs regarding the dependency on endogenous PGs/IP receptors and TRPV1. It is assumed that lafutidine interacts with CSN at yet unidentified sites other than TRPV1.

Aldo-keto reductase family member C3(AKR1C3)promotes hepatocellular carcinoma cell growth by producing prostaglandin F2α

Hepatocellular carcinoma(HCC)is a leading cause of death worldwide.Current therapies are effective for HCC patients with early disease,but many patients suffer recurrence after surgery and have a poor response to chemotherapy.Therefore,new therapeutic targets are needed.We analyzed gene expression profiles between HCC tissues and normal adjacent tissues from public databases and found that the expression of genes involved in lipid metabolism was significantly different.The analysis showed that AKR1C3 was upregulated in tumors,and high AKR1C3 expression was associated with a poorer prognosis in HCC patients.In vitro,assays demonstrated that the knockdown of AKR1C3 or the addition of the AKR1C3 inhibitor indomethacin suppressed the growth and colony formation of HCC cell lines.Knockdown of AKR1C3 in Huh7 cells reduced tumor growth in vivo.To explore the mechanism,we performed pathway enrichment analysis,and the results linked the expression of AKR1C3 with prostaglandin F2 alpha(PGF2a)downstream target genes.Suppression of AKR1C3 activity reduced the production of PGF2a,and supplementation with PGF2a restored the growth of indomethacin-treated Huh7 cells.Knockdown of the PGF receptor(PTGFR)and treatment with a PTGFR inhibitor significantly reduced HCC growth.We showed that indomethacin potentiated the sensitivity of Huh7 cells to sorafenib.In summary,our results indicate that AKR1C3 upregulation may promote HCC growth by promoting the production of PGF2α,and suppression of PTGFR limited HCC growth.Therefore,targeting the AKR1C3-PGF2a-PTGFR axis may be a new strategy for the treatment of HCC.

Pathogenesis of chronic enteropathy associated with the SLCO2A1 gene:Hypotheses and conundrums

Chronic enteropathy associated with the SLCO2A1 gene(CEAS)is a complex gastroenterological condition characterized by multiple ulcers in the small intestine with chronic bleeding and protein loss.This review explores the potential mechanisms underlying the pathogenesis of CEAS,focusing on the role of SLCO2A1-encoded prostaglandin transporter OATP2A1 and its impact on prostaglandin E2(PGE2)levels.Studies have suggested that elevated PGE2 levels contribute to mucosal damage,inflammation,and disruption of the intestinal barrier.The effects of PGE2 on macrophage activation and Maxi-Cl channel functionality,as well as its interaction with nonsteroidal anti-inflammatory drugs play crucial roles in the progression of CEAS.Understanding the balance between its protective and pro-inflammatory effects and the complex interactions within the gastrointestinal tract can shed light on potential therapeutic targets for CEAS and guide the development of novel,targeted therapies.

Prostaglandin E1 administration post liver transplantation and renal outcomes:A retrospective single center experience

BACKGROUND Prostaglandin E1(PGE1),or alprostadil,is a potent vasodilator that improves hepatic blood flow and reduces ischemia-reperfusion injury post-liver transplantation(LT).However,the benefits of PGE1 on renal function after LT have not yet been well described.AIM To assess the impact of PGE1 administration on renal function in patients who underwent liver or liver-kidney transplant.METHODS This retrospective study included all patients who underwent liver or liverkidney transplant at our institution from January,2011 to December,2021.Patients were classified based on whether they received PGE1.PGE1 was administered post-LT to those with transaminases>1000 U/L in the immediate postoperative period.Demographics,post-LT treatments and/or complications,renal function,and survival were analyzed.Multivariable logistic regression analysis was performed,and a two-tailed P value<0.05 was considered statistically significant.RESULTS A total of 145 patients underwent LT,with 44(30%)receiving PGE1.Baseline patient characteristics were comparable,except the PGE1 group had significantly higher aspartate aminotransferase(AST)(1961.9 U/L±1862.3 U/L vs 878 U/L±741.4 U/L,P=0.000),alanine aminotransferase(1070.6 U/L±895 U/L vs 547.7 U/L±410 U/L,P=0.000),international normalized ratio on post-LT day 1(2±0.74 vs 1.8±0.4,P=0.03),a longer intensive care unit stay(8.1 days±11.8 days vs 3.8 days±4.6 days,P=0.003),more vasopressor use(55.53 hours±111 hours vs 16.33 hours±26.3 hours,P=0.002),and higher immediate postoperative complications(18.6%vs 4.9%,P=0.04).The PGE1 group also had a significantly higher 90-day readmission rate(29.6%vs 13.1%,P=0.02)and lower 1-year liver graft survival(87.5%vs 98.9%,P=0.005).However,30-day readmission(31.6%vs 27.4%,P=0.64),LT complications(hepatic artery thrombosis,biliary complications,rejection of liver graft,cardiomyopathy),1-year patient survival(96.9%vs 97.8%,P=0.77),overall liver graft survival,and overall patient survival were similar between the two groups(95.4%vs 93.9%,P=0.74 and 88.4%vs 86.9%,P=0.81 respectively).Although the PGE1 group had a significantly lower glomerular filtration rate(eGFR)on post-LT day 7(46.3 mL/minute±26.7 mL/minute vs 62.5 mL/minute±34 mL/minute,P=0.009),the eventual need for renal replacement therapy(13.6%vs 5.9%,P=0.09),the number of dialysis sessions(0.91 vs 0.27,P=0.13),and eGFR at 1-month(37.2 mL/minute±35.9 mL/minute vs 42 mL/minute±36.9 mL/minute,P=0.49),6-months(54.8 mL/minute±21.6 mL/minute vs 62 mL/minute±21.4 mL/minute,P=0.09),and 12-months(63.7 mL/minute±20.7 mL/minute vs 62.8 mL/minute±20.3 mL/minute,P=0.85)post-LT were similar to those in the non-PGE1 group.CONCLUSION In patients who received PGE1 for ischemia-reperfusion injury,despite immediate acute renal injury post-LT,the renal function at 1-month,6-months,and 12-months post-LT was similar compared to those without ischemiareperfusion injury.Prospective clinical trials are needed to further elucidate the benefits of PGE1 use in renal function.

ANISODAMINE INHIBITS ENDOTOXIN-INDUCED PROSTAGLANDINS AND LEUKOTRIENES RELEASE FROM MOUSE MACROPHAGES

It was reported that anisodamine (654-2)reduced thromboxane synthesis by platelets and lowered the plasma prostaglandin level in endotoxic shock animals when administered in the early phase of shock. However, the exact relationship between arachidonic acid (AA) metabolism and the effects of 654-2 has not been completely understood. We found that 654-2 decreased acetylcholine-and norepinephrine-induced PG release from rabbit iris,

THE EFFECT OF AMMONIUM GLYCYR-RHIZINATE ON THE BIOSYNTHESIS OF PROSTAGLANDINS E_2 AND F_(2a)

Ammonium glycyrrhizinate is the amide of glycyrrhetinic acid which derives from the glycyrrhizin, the effective component of glycyrrhiza. Recent studies have proved that ammonium glycyrrhizinate plays an important role in some vital pharmacological processes, like immunoregulation. In order to study the mechanisms of action of ammonium glycyrrhizinate at the enzyme molecular level, in this note,

Acute Uveitis in Neovascular Glaucoma Patient after a Single Dose of Travoprost

A 38-year-old man with no history of uveitis developed neovascular glaucoma (NVG) due to proliferative diabetic retinopathy (PDR). He had a history of ocular surgery with placement of glaucoma drainage implants (GDI), ultrasonic phacoemulsification, and intraocular lens implantation in both eyes. The patient had undergone a recent pars plana vitrectomy with complete panretinal photocoagulation (PRP) to clear vitreous hemorrhage in his right eye. To prevent progressive optic nerve damage, travoprost was tentatively administered because of inadequate intraocular pressure (IOP) control following surgery, laser treatment, and topical administration of many other IOP-lowering drugs. The patient experienced severe vision loss associated with acute anterior and intermediate uveitis. We consider it a rare complication due to the NVG patient’s vulnerability following ocular surgery. Given that acute uveitis developed rapidly and required time to resolve, systemic corticosteroid treatment could be considered to accelerate the resolution of inflammation.

Neuroaxonal and cellular damage/protection by prostanoid receptor ligands,fatty acid derivatives and associated enzyme inhibitors

Cellular and mitochondrial membrane phospholipids provide the substrate for synthesis and release of prostaglandins in response to certain chemical,mechanical,noxious and other stimuli.Prostaglandin D_(2),prostaglandin E_(2),prostaglandin F_(2)α,prostaglandin I_(2)and thromboxane-A_(2)interact with five major receptors(and their sub-types)to elicit specific downstream cellular and tissue actions.In general,prostaglandins have been associated with pain,inflammation,and edema when they are present at high local concentrations and involved on a chronic basis.However,in acute settings,certain endogenous and exogenous prostaglandins have beneficial effects ranging from mediating muscle contraction/relaxation,providing cellular protection,regulating sleep,and enhancing blood flow,to lowering intraocular pressure to prevent the development of glaucoma,a blinding disease.Several classes of prostaglandins are implicated(or are considered beneficial)in certain central nervous system dysfunctions(e.g.,Alzheimer’s,Parkinson’s,and Huntington’s diseases;amyotrophic lateral sclerosis and multiple sclerosis;stroke,traumatic brain injuries and pain)and in ocular disorders(e.g.,ocular hypertension and glaucoma;allergy and inflammation;edematous retinal disorders).This review endeavors to address the physiological/pathological roles of prostaglandins in the central nervous system and ocular function in health and disease,and provides insights towards the therapeutic utility of some prostaglandin agonists and antagonists,polyunsaturated fatty acids,and cyclooxygenase inhibitors.

Hepatic ischemia-reperfusion syndrome and its effect on the cardiovascular system: The role of treprostinil, a synthetic prostacyclin analog

Hepatic ischemia-reperfusion syndrome has been the subject of intensive study and experimentation in recent decades since it is responsible for the outcome of several clinical entities,such as major hepatic resections and liver transplantation.In addition to the organ’s post reperfusion injury,this syndrome appears to play a central role in the dysfunction of distant tissues and systems.Thus,continuous research should be directed toward finding effective therapeutic options to improve the outcome and reduce the postoperative morbidity and mortality rates.Treprostinil is a synthetic analog of prostaglandin I2,and its experimental administration has shown encouraging results.It has already been approved by the Food and Drug Administration in the United States for pulmonary arterial hypertension and has been used in liver transplantation,where preliminary encouraging results showed its safety and feasibility by using continuous intravenous administration at a dose of 5 ng/kg/min.Treprostinil improves renal and hepatic function,diminishes hepatic oxidative stress and lipid peroxidation,reduces hepatictoll-like receptor 9 and inflammation,inhibits hepatic apoptosis and restores hepatic adenosine triphosphate(ATP)levels and ATP synthases,which is necessary for functional maintenance of mitochondria.Treprostinil exhibits vasodilatory properties and antiplatelet activity and regulates proinflam-matory cytokines;therefore,it can potentially minimize ischemia-reperfusion injury.Additionally,it may have beneficial effects on cardiovascular parameters,and much current research interest is concentrated on this compound.

Prostaglandin F_(2α)synthase promotes oxaliplatin resistance in colorectal cancer through prostaglandin F_(2α)-dependent and F_(2α)-independent mechanism

BACKGROUND Oxaliplatin(Oxa)is the first-line chemotherapy drug for colorectal cancer(CRC),and Oxa resistance is crucial for treatment failure.Prostaglandin F_(2α)synthase(PGF 2α)(PGFS),an enzyme that catalyzes the production of PGF_(2α),is involved in the proliferation and growth of a variety of tumors.However,the role of PGFS in Oxa resistance in CRC remains unclear.AIM To explore the role and related mechanisms of PGFS in mediating Oxa resistance in CRC.METHODS The PGFS expression level was examined in 37 pairs of CRC tissues and paracancerous tissues at both the mRNA and protein levels.Overexpression or knockdown of PGFS was performed in CRC cell lines with acquired Oxa resistance(HCT116-OxR and HCT8-OxR)and their parental cell lines(HCT116 and HCT8)to assess its influence on cell proliferation,chemoresistance,apoptosis,and DNA damage.For determination of the underlying mechanisms,CRC cells were examined for platinum-DNA adducts and reactive oxygen species(ROS)levels in the presence of a PGFS inhibitor or its products.RESULTS Both the protein and mRNA levels of PGFS were increased in the 37 examined CRC tissues compared to the adjacent normal tissues.Oxa induced PGFS expression in the parental HCT116 and HCT8 cells in a dosedependent manner.Furthermore,overexpression of PGFS in parental CRC cells significantly attenuated Oxainduced proliferative suppression,apoptosis,and DNA damage.In contrast,knockdown of PGFS in Oxa-resistant HCT116 and HCT8 cells(HCT116-OxR and HCT8-OxR)accentuated the effect of Oxa treatment in vitro and in vivo.The addition of the PGFS inhibitor indomethacin enhanced the cytotoxicity caused by Oxa.Treatment with the PGFS-catalyzed product PGF_(2α)reversed the effect of PGFS knockdown on Oxa sensitivity.Interestingly,PGFS inhibited the formation of platinum-DNA adducts in a PGF_(2α)-independent manner.PGF_(2α)exerts its protective effect against DNA damage by reducing ROS levels.CONCLUSION PGFS promotes resistance to Oxa in CRC via both PGF_(2α)-dependent and PGF_(2α)-independent mechanisms.

The antioxidant trolox inhibits aging and enhances prostaglandin E-2 secretion in mesenchymal stem cells

Mesenchymal stem cells(MSCs)have been widely used in regenerative medicine and clinical therapy due to their capabilities of proliferation,differentiation,and immune regulation.However,during in vitro expansion,MSCs are prone to aging,which largely limits their application.Prostaglandin E-2(PGE-2)is a key effector secreted by MSCs to exert immunomodulatory effects.By screening the compound library for PGE-2 secretion,the antioxidant trolox was verified as a stimulator of MSCs to secrete PGE-2.The effect of antioxidant trolox on biological characteristics of MSCS,including aging,proliferation,and gene expression,was examined.The results demonstrated that trolox can resist aging,promote proliferation,and enhance PGE-2 secretion of MSCs without affecting their surface marker expression.Furthermore,trolox treatment up-regulates miR-17-92 clusters in MSCs and may contribute to its anti-aging effects.Thus,trolox addition might be beneficial for MSCs expansion and their application.

Intra-arterial lipo-prostaglandin E1 infusion for arterial spasm in liver transplantation:A case report

BACKGROUND Hepatic artery obstruction is a critical consideration in graft outcomes after living donor liver transplantation.We report a case of diffuse arterial vasospasm that developed immediately after anastomosis and was managed with an intra-arterial infusion of lipo-prostaglandin E1(PGE1).CASE SUMMARY A 57-year-old male with hepatitis B virus-related liver cirrhosis and hepatocellular carcinoma underwent ABO-incompatible living donor liver transplant.The grafted hepatic artery was first anastomosed to the recipient’s right hepatic artery stump.However,the arterial pulse immediately weakened.Although a new anastomosis was performed using the right gastroepiploic artery,the patient’s arterial pulse rate remained poor.We attempted angiographic intervention immediately after the operation;it showed diffuse arterial vasospasms like‘beads on a string’.We attempted continuous infusion of lipo-PGE1 overnight via an intra-arterial catheter.The next day,arterial flow improved without any spasms or strictures.The patient had no additional arterial complications or related sequelae at the time of writing,1-year post-liver transplantation.CONCLUSION Angiographic evaluation is helpful in cases of repetitive arterial obstruction,and intra-arterial infusion of lipo-PGE1 may be effective in treating diffuse arterial spasms.

丹参的多种临床应用

丹参的多种临床应用曹元成，马英玲丹参，苦能降泄，微寒清热，入心、肝二经血分，而有活血祛瘀、凉血消肿、清心除烦等作用。前人认为丹参能“补血”，而有“一味丹参，功同四物”的说法，其实为祛瘀通经之品，所谓能够“补血”，实为“瘀血法则新血生”之义。在临床上有...

西黄丸联合紫杉醇抑制人乳腺癌细胞MDA-MB-231的作用机制研究

目的研究西黄丸(Xihuang wan,XHW)联合紫杉醇(paclitaxel,PTX)对人乳腺癌细胞MDA-MB-231增殖、凋亡的影响及其分子机制。方法首先,通过低温浸提法获得西黄丸浸液,用不同浓度的西黄丸浸液单独或联合紫杉醇处理MDA-MB-231细胞系,通过CCK8实验检测细胞增殖,流式细胞术检测其凋亡的变化,ELISA检测细胞上清中前列腺素E2(prostaglandin E2,PGE2)含量。结果单独使用西黄丸即可抑制MDA-MB-231增殖,联用紫杉醇抑制细胞增殖效果更明显;单用西黄丸可诱导MDA-MB-231凋亡,联用紫杉醇诱导凋亡效果也可获得提高;紫杉醇会诱导细胞外液中PGE2含量升高,联用西黄丸可降低升高的PGE2。结论西黄丸联合紫杉醇可更好地诱导人乳腺癌细胞系MDA-MB-231发生凋亡并抑制其增殖,同时还可以抑制受紫杉醇诱导而升高的PGE2,这可能是西黄丸联用化疗药防止肿瘤复发、转移的重要分子机制之一。