Effect of lysophosphatidic acid on hepatoma cells and related mechanism / 临床肝胆病杂志

ObjectiveTo investigate the expression of lysophosphatidic acid （LPA） in patients with liver cancer， as well as its influence on malignant biological behavior of liver cancer and related regulatory mechanism. MethodsFrom January 2016 to December 2022， 26 patients with liver cancer， 28 patients with liver cirrhosis， and 28 individuals undergoing physical examination were enrolled. ELISIA was used to measure the content of LPA in plasma and peritoneal effusion of the patients with liver cancer or liver cirrhosis accompanied by peritoneal effusion， and the content of LPA was measured in plasma of the normal population at the same time， so as to clarify the difference in the expression of LPA in different populations， such as the patients with liver cancer and those with liver cirrhosis. MTT cell proliferation assay and cell migration assay were used to observe the influence of LPA and its inhibitor pertussis toxin （PTX） on the proliferation， migration， and invasion of SMMC7721 cells. In order to investigate the effect of LPA on the expression of RhoA and its upstream and downstream molecules FAK and P53 after binding to its receptor， qPCR and Western blot were used to observe the effect of LPA on the mRNA and protein expression levels of P53， FAK， and RhoA in SMMC7721 cells. A one-way analysis of variance was used for comparison of the means of continuous data between multiple groups， and the SNK-q test was used for comparison between two groups. ResultsCompared with the patients with liver cirrhosis， the patients with liver cancer had a significantly higher concentration of LPA in plasma （4.99±0.55 μmol/L vs 2.63±0.43 μmol/L， P<0.05） and peritoneal effusion （5.19±0.63 μmol/L vs 2.91±0.46 μmol/L， P<0.05）， and the patients with liver cancer also had a significantly higher level of plasma LPA than the normal population （4.99±0.55 μmol/L vs 1.61±0.39 μmol/L， P<0.05）. The cell proliferation assay showed that LPA significantly promoted the proliferation of SMMC7721 cells， and cell proliferation rate increased with the increase in dose and time； in particular， the middle-and high-dose groups had a significantly higher proliferation rate than the control group （P<0.05）. PTX inhibited the proliferative capacity of SMMC7721 cells in a time-dependent manner， and there was a significant difference between the groups （P<0.05）. The proliferation rate of the 72-hour high-dose LPA group was 3.6 times that of the control group， while the proliferation rate of the PTX group was 0.6 times that of the control group； the proliferation rate of the 72-hour high-dose LPA+PTX group was 1.2 times that of the control group. In addition， LPA increased the migration ability of hepatoma cells， while PTX inhibited their migration， in a time-dependent manner， and there was a significant difference between the groups （P<0.05）. The migration rate of the 72-hour high-dose LPA group was 3.09 times that of the control group， while the migration rate of the PTX group was 0.4 times that of the control group； the migration rate of the 72-hour high-dose LPA+PTX group was 0.99 times that of the control group. qPCR and Western blot showed that there were significant reductions in the mRNA and protein expression levels of P53 in SMMC7721 cells after LPA treatment， while there were significant increases in the mRNA and protein expression levels of FAK and RhoA； there was a significant difference between the LPA group and the control group （P<0.05）. ConclusionThere is an abnormal increase in the expression of LPA in patients with liver cancer， and LPA can promote the proliferation of liver cancer cells and increase their migration ability. At the same time， LPA changes the expression levels of P53， FAK， and RhoA， which may be associated with the promotion of tumor development and progression by LPA.

Effect of STAT3 on Lysophosphatidic Acid-Induced Oral Cancer Cell Invasion / 치위생과학회지

BACKGROUND: Oral cancer has a high incidence worldwide and has been closely associated with smoking, alcohol, and infection by the human papillomavirus. Metastasis is highly important for oral cancer survival. Lysophosphatidic acid (LPA) is a bioactive lipid mediator that promotes various cellular processes, including cell survival, proliferation, metastasis, and invasion. Signal transducer and activator of transcription (STATs) are transcription factors that mediate gene expression. Among the seven types of STATs in mammals, STAT3 is involved in invasion and metastasis of numerous tumors. However, little is known about the role of STAT3 in oral tumor invasion. In the present study, we hypothesized that STAT3 mediates LPA-induced oral cancer invasion. METHODS: Immunoblotting was performed to analyze LPA-induced STAT3 activation. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was performed to assess the survival rates of YD-10B cells. STAT3 levels in LPA-treated oral tumor cells were evaluated by performing in vitro invasion assay. RESULTS: To the best of our knowledge, this is the first study to demonstrate that LPA enhances STAT3 phosphorylation in oral cancer. In addition, treatment with WP1066, a selective inhibitor of STAT3, at a concentration that does not cause severe reduction in cell viability, significantly attenuated LPA-induced YD-10B cancer cell invasion. CONCLUSION: The results suggested that LPA induces oral tumor cells with greater invasive potential via STAT3 activation. Our findings provided important insights into the mechanisms underlying mouth neoplasms.

Effect of Resveratrol on Oral Cancer Cell Invasion Induced by Lysophosphatidic Acid / 치위생과학회지

The aim of the current study was to demonstrate the potential therapeutic efficacy of resveratrol in oral cancer patients. Lysophosphatidic acid (LPA) intensifies cancer cell invasion and metastasis, whereas resveratrol, a natural polyphenolic compound, possesses antitumor activity, suppressing cell proliferation and progression in various cancer cell lines (ovarian, gastric, oral, pancreatic, colon, and prostate cancer cells). In addition, resveratrol has been identified as an inhibitor of LPA-induced proteolytic enzyme expression and ovarian cancer invasion. Furthermore, resveratrol was shown to inhibit oral cancer cell invasion by downregulating hypoxia-inducible factor 1α and vascular endothelial growth factor expression. Recently, we demonstrated that LPA is important for the expression of transcription factors TWIST and SLUG during epithelial-mesenchymal transition (EMT) in oral squamous carcinoma cells. In this study, we treated serum-starved cultures of oral squamous carcinoma cell line YD-10B with resveratrol for 24 hours prior to stimulation with LPA. To identify an optimal resveratrol concentration that does not induce apoptosis in oral squamous carcinoma cells, we determined the toxicity of resveratrol in YD-10B cells by assessing their viability using the MTT assay. Another assay was performed using Matrigel-coated cell culture inserts to detect oral cancer cell invasion activity. Immunoblotting was applied for analyzing protein expression of SLUG, TWIST1, E-cadherin, and GAPDH. We demonstrated that resveratrol efficiently inhibited LPA-induced oral cancer cell EMT and invasion by downregulating SLUG and TWIST1 expression. Therefore, resveratrol may potentially reduce oral squamous carcinoma cell invasion and metastasis in oral cancer patients, improving their survival outcomes. In summary, we identified new targets for the development of therapies against oral cancer progression and characterized the therapeutic potential of resveratrol for the treatment of oral cancer patients.

Effects of ibuprofen on the growth and development of oligodendrocytes / 天津医药

Objective To study the effects of ibuprofen on the growth and development of oligodendrocytes. Methods A total of 6 clean and healthy adult female SD (Sprague Dawley) rats were used for extracting and culturing of oligodendrocytes(OLs).Lysophosphatidic acid(LPA)was then added,and the morphological changes of OLs pre-treatment and post-treatment were observed. Then 6 newborn rats (born 24-48 h) were used for mixed glial cell extraction from the cortex, then the OPCs were inoculated into the culture plates and randomly divided into control group, ibuprofen group, lysophosphatidic acid(LPA)group and LPA+ibuprofen group.After the adhering of the cells in each group for three days, cell morphology was observed,and the drugs were added as interventions.The control group was treated with normal saline, and the other 3 groups were added with saline solution of ibuprofen(100 μmol/L),LPA(1.0 μmol/L)and the mixture of them. The cell morphological changes were observed after 7-day intervention.The morphology of OPCs and OLs were observed by immunofluorescence staining through OPCs'specific immune markers (platelet-derived growth factor receptor alpha, PDGFR-α)and OLs'specific immune markers(myelin basic protein,MBP)along with cell count of mature OLs.Western blot assay was used to detect the relative expression level of MBP in each group. Results After the treatment with LPA to the mature OLs,protrusions were shrinking and became very sparse.The morphology of cells developed well in each group after cell adhering for 3 days. After drug intervention for 7 days, more cell protrusions and branches were observed in ibuprofen group and LPA+ibuprofen group than those of the control group and LPA group.The results of cell count showed that the number of MBP positive cells was significantly higher in the ibuprofen group and LPA+ibuprofen group than that in the control group and LPA group(P<0.01).The results of Western blot assay showed that the MBP protein expression was significantly less in LPA group than the other three groups (P<0.01), and the expression was significantly higher in the ibuprofen group than that of LPA+ibuprofen group (P<0.01). Conclusion LPA has a toxic effect on the growth and development of OPCs, and it has an inhibitory effect on the normal growth of mature OLs. A certain concentration of ibuprofen can significantly inhibit the cytotoxicity of LPA on OPCs and OLs,and promote the formation and maintenance of mature OLs.

Lysophosphatidic Acid-Induced TWIST1 and Slug Expression in Oral Cancer Cell Invasion / 치위생과학회지

Relative to its incidence, oral cancer has serious negative social effects. The exact causes of oral cancer have not been clarified, but many studies have implicated smoking and drinking. However, the fundamental mechanism of oral cancer causation has yet to be elucidated. Lysophosphatidic acid (LPA) augments epithelial mesenchymal transition (EMT) and development of various cancer cells. However, a detailed mechanistic explanation for LPA-induced EMT and the effects of EMT-promoting conditions on oral squamous cell carcinoma development remain elusive. In the present study, a quantitative reverse transcription polymerase chain reaction was used to analyze TWIST1, Slug, E-cadherin, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) transcript expression. Immunoblotting was used to analyze TWIST1, Slug, E-cadherin, and GAPDH protein expression. siRNAs were used to silence TWIST1 and Slug transcript expression. A matrigel-coated in vitro invasion insert was used to analyze oral cancer cell invasion. The results of the present study show that the expression levels of TWIST1 and Slug, which are EMT factors, were increased by LPA treatment in YD-10B oral squamous cell carcinoma. Conversely, E-cadherin expression was significantly reduced. In addition, transfection of the cells with TWIST1 and Slug siRNA strongly inhibited LPA-induced oral cancer cell invasion. The present study shows that TWIST1 and Slug mediate LPA-induced oral cancer cell EMT and invasiveness. The present study confirmed the mechanism by which LPA promotes oral cancer cell development, with TWIST1 and Slug providing novel biomarkers and promising therapeutic targets for oral cancer cell development.

The clinical study on the correlation of lysophosphatidic acid and vascular endotheli growth factor and endothelin in serum of pneumoconiosis / 中华劳动卫生职业病杂志

Objective@#To explore the role of lysophosphatidic acid, vascular endothelial growth facor and endothelin in the pathogenesis of pulmonary fibrosis in coal workers’pneumoconiosis patients, the relationship of lysophosphatidic acid, VEGF and ET in serum was studied.@*Methods@#Sixty two pneumoconiosis patients were selected as cases group, which included 23 cases of stage Ⅰ, 25 cases of stageⅡand 14 cases of stageⅢ. Twenty workers were selected as dust exposure group who exposed to coal dust for more than 2 years and had not been diagnosed as pneumoconiosis. Ten healthy people who had no occupational dust exposure were simultaneously selected as the control group. The serum levels of LPA, VEGF and ET were measured by ELISA.@*Results@#The serum levels of VEGF and ET in coal dust exposed group and pneumoconiosis group were much higher than in the control group. The differences were statistically significant among the three groups (P<0.01) . The serum levels of LPA increased in the dust exposed group, stage Ⅰand stage Ⅱgroup. The serum levels of LPA correlated positively with the levels of VEGF and ET (P<0.05) .@*Conclusions@#The serum levels of LPA, VEGF and ET had evident correlation with the pulmonary fibrosis caused by coal dust, which indicate that LPA, VEGF and ET may play a pivotal role in the process of pulmonary fibrosis. The study will throw light on both pathogenesis and early intervention for pneumoconiosis.

The relationship between the apolipoprotein M-sphingosine-1-phosphate axis and atherosclerosis / 中华检验医学杂志

Apolipoprotein M-sphingosine-1-phosphate axis ( apoM-S1P axis ) signaling pathway consists of apolipoproteinM (apoM), sphingosine-1-phosphate (S1P) and sphingosine-1-phosphate receptor (S1PR).Plasma apoM belongs to lipocalinsuperfamily members , and is mainly associated to high density lipoprotein( HDL), whereas HDL-cholesterol correlates inversely with cardiovascular risk .The ability of apoM to bind S1P is due to a lipophilic binding pocket within the lipocalin structure of the apoM molecule . S1P, a bioactive mediator of phospholipid metabolism , predominantly abound in HDL among all lipoproteins.S1P can not only be used as intracellular second messengers , but also as intercellular signal molecules, activating of G protein-coupled receptors (S1PR) to mediate various physiological functions.It′s clear that apoM protects human beings from atherosclerosis .Furthermore, recent studies showed that S1P has a significant impact on atherosclerosis , and ApoM-S1P axis may play a important role in the pathogenesis or progression of atherosclerosis .

Study on the correlation between plasma lysophosphatidic acid, matrix metalloproteinase 9 and stability of carotid artery plaque in silent cerebral infarction / 中国医师进修杂志

Objective To investigate the correlation between plasma lysophosphatidic acid (LPA),matrix metalloproteinase 9 (MMP-9) and stability of carotid artery plaque in silent cerebral infarction (SCI).Methods According to the results of the ultrasound examination of carotid,128 patients with SCI were divided into intima-media thickness (IMT) normal group (35 cases),IMT thickening group (50 cases),stable plaque group (24 cases) and unstable plaque group (19 cases),and 40 healthy cases were selected as control group.The levels of plasma LPA and MMP-9 were determined and compared.Results The levels of plasma MMP-9 and LPA in IMT normal group,IMT thickening group,stable plaque group and unstable plaque group were higher than those in control group [(162.31 ±21.79),(219.62 ±32.51),(279.11 ±36.83),(382.43 ±41.92) μg/L vs.(96.54 ±21.34) μg/L and (1.91 ±0.42),(2.15 ±0.39),(2.69 ±0.51),(3.27 ± 0.48) μ mol/L vs.(1.69 ± 0.26) μ mol/L],and there were significant differences (P ＜ 0.01).In IMT normal group,IMT thickening group,stable plaque group and unstable plaque group,the levels of plasma MMP-9 and LPA gradually increased,and the differences among the groups were statistically significant (P ＜ 0.01).The correlation analysis showed that the levels of plasma MMP-9,LPA and IMT of carotid had positive correlation (r =0.713,P ＜ 0.01 ; r =0.679,P ＜ 0.01).Conclusion The levels of plasma MMP-9 and LPA can reflect IMT of carotid and plaque stability in some extent,which can provide the clinical basis for condition assessment,prevention and treatment of SCI patients.

Effects of plasma from patients with preeclampsia on the proliferation and apoptosis of human umbilical vein endothelial cells and its relationship with lysophosphatidic acid receptors / 中华妇产科杂志

Objectives To investigate the effects of plasma from the patients with preeclampsia on proliferation and apoptosis of human umbilical vein endothelial cells(HUVEC),and to explore the relationship between cell damage and lysophosphatidic acid(LPA)receptors.Methods Sixty patients with preeclampsia were recruited from October 2011 to June 2012 in the First Affilated Hospital of Zhengzhou University.Among them,thirty cases were defined as the mild preeclampsia group and thirty cases were defined as the severe preeclampsia group.The other thirty healthy pregnant women were recruited in the healthy pregnant women group.The levels of plasma LPA in the three groups were measured.The HUVEC were cultured in vitro with plasma from the three groups,and a blank control group was set up as well.Proliferation and apoptosis of HUVEC were measured by MTT assay and flow cytometry.Immunohistochemistry of biotin streptomyces protein peroxidase(SP)method was used to measure the protein expression level of Edg 2,4,7.Results(1)The plasma LPA levels in the healthy pregnant woman group,mild preeclampsia group and severe preeclampsia group were(3.38 ± 2.08)μmol/L,(6.12 ± 0.22)μmol/L,(9.10 ± 0.17)μmol/L,respectively.The plasma levels of LPA in patients with preeclampsia were significantly higher than that in the healthy pregnant women(P ＜ 0.01).(2)The proliferation rate of HUVEC in the mild and severe preeclampsia groups [(65.2 ± 2.7)％ and(51.9 ± 2.8)％] were significantly lower than that in the healthy pregnant women group and the control group [(84.3 ± 3.1)％ and(100.0 ± 0.0)％,P ＜ 0.01].(3)The early apoptosis rate,middle-late apoptosis rate and total apoptosis rate of HUVEC in the mild and severe preeclampsia groups [total apoptosis rate were(30.4 ±2.0)％ and(43.4 ±2.5)％] were significantly higher than those in the healthy pregnant women group and the control group [total apoptosis rate were(18.6 ± 1.6)％ and(8.0 ± 1.5)％,P ＜ 0.01].(4)The expression positive rates of Edg 2,4,7 proteins in the four groups were as following:mild preeclampsia group 83％,80％ and 73％;severe preeclampsia group 97％,93％ and 90％;healthy pregnant women group 40％,40％ and 37％,and the control group 10％,10％ and 7％ respectively.The positive rates of HUVEC in the mild and severe preeclampsia groups were significantly higher than those in the healthy pregnant women group and the control group(P ＜ 0.01).Conclusions The plasma of patients with preeclampsia could inhibit proliferation and promote apoptosis of HUVEC,and induce the expression of Edg 2,4,7 proteins.It suggested that the increase of lysophosphatidic acid in plasma could be one of the reasons of endothelial cell damage in patients with preeclampsia.

Relationship of lysophosphatidic acid and matrix metalloproteinase-9 with carotid atheromatous plaque stability in patients with cerebral infarction / 中华老年医学杂志

Objective To investigate the correlation of plasma lysophosphatidic acid (LPA) and matrix metalloproteinase-9 (MMP-9) with carotid atheromatous plaque stability in patients with cerebral infarction. Methods The duplex uhrasonography and transcranial Doppler-detected microemboli were performed in the carotid arteries of all the 87 patients with cerebral infarction located in arteriae carotis interna system. The patients were divided into the intima thickening group (n=16),unstable plaque group (n=41), stable plaque group (n=21) and non-plaque group (n=9). And there were 27 patients with positive microembolic signal and 60 patients with negative microembolic signal.The plasma levels of LPA and MMP-9 were determined by quantitative determination of inorganic phosphorus and enzyme-linked immunosorbent assay. Results The levels of LPA and MMP-9 were significantly higher in unstable plaque group than in the other three groups (F=49.98 and 106.49,both P<0.01), MMP-9 in intima thickening group and stable plaque group were both higher than in non-plaque group (q=7.04 and 7.51, both P=0. 00). LPA was higher in intima thickening group than in stable plaque group (q=7.37, P=0. 00), and higher in the above two groups than in non-plaque group (both P<0.05). The levels of LPA and MMP-9 were higher in microembolic signal-positive patients than in signal-negative patients (t=42.57 and 16.61, both P=0.00). LPA level was positively correlated with MMP-9 (r=0.22, P<0.05). Conclusions LPA and MMP-9 may serve as a potential risk signal to hint the formation and rupture of unstable carotid atheromatous plaque which may cause ischemic cerebrovascular disease.

Lysophosphatidic acid and tumor / 国际肿瘤学杂志

Lysophosphatidic acid (LPA) is a newly discovered multi-function "phospholipid messenger" which is primarily from platelet activation,and is involved in a variety of biological effects,and closely correlated with carcinoma growth,invasion and metastasis.LPA plays an important role in carcinoma development.There is a certain degree of clinical significance of LPA in some carcinoma diagnosis and prognosis.

Changes of plasma lysophosphatidic levels in patients with obstructive sleep apnea syndrome-associated acute cerebral infarction / 中国综合临床

Objective To observe the changing characteristics of plasma lysophosphatidic acid (LPA) or acidia phospholipid (AP) levels in patients with obstructive sleep apnea syndrome-associated(OSAS)acute cerebral infarction and to explore the pathophysiological mechanisms of OSAS-related stroke so as to provide basis for clinical antithrombotic therapy. Methods Thirty-six patients of OSAS, 32 patients of OSAS-related acute stoke and 36 patients of acute stoke without OSAS diagnosed by clinical and accessory examinations were enrolled in the current study. Thirty-eight age-matched healthy subjects were recruited as controls. The changes of the plasma LPA and AP levels were measured. Results Within 24 hours after symptom onset, the plasma LPA and AP levels in the OSAS-related acute cerebral infarction group (LPA(3. 78 ±0. 56) μmol/L; AP(7. 63 ± 1. 38) μmol/L) were significantly higher than those in the OSAS group(LPA(3. 17 ±0. 65) μmol/L; AP(6. 60 ± 1. 20) μmol/L) ,the not OSAS-related acute cerebral infarction group (LPA (3. 40 ± 0. 59)μmol/L; AP (6. 41 ± 1. 37)μmol/L) and the control group (LPA(2.76±0.45)μmol/L;AP(4.52±0. 83) μmol/L (P < 0. 01)) . The levels of LPA and AP in the OSAS group and the not OSAS-related acute cerebral infarction group were significantly higher than those in the control group(P<0. 01). Seven days after symptom onset, the plasma LPA and AP levels in the OSAS-associated acute cerebral infarction group (LPA(3.08 ± 0. 58) μmol/L; AP(6. 15 ±1. 14)μmol/L) were still higher(P < 0. 01) . The plasma LPA levels were not significantly different among the OSAS-related acute cerebral infarction group, the not OSAS-related acute cerebral infarction group and the control group 21 days after symptom onset, whereas the plasma AP levels in the OSAS-related acute cerebral infarction group (5. 04 ± 0. 83) μmol/L were still significantly higher than those in the not OSAS-related acute cerebral infarction group (4. 57 ± 0. 94) μmol/L and the control group (P < 0.05). Conclusions The significantly elevated plasma LPA and AP levels in patients with OSAS suggested that platelets in vivo are in an activated state and in cerebral ischemia and hypoxia state, especially for the OSAS-related acute cerebral infarction patients. The activated state of platelet may persist for a long time, thus the time window for antithrombotic therapy may be longer.

Elevated plasma lysophosphatidic acid levels and risk of silent brain infarction in patients with atrial fibrillation / 中华神经科杂志

Objective To investigate the changes of plasma lysephosphatidic acid (LPA) or acidic phospholipids (AP) levels in patients with nonvalvular atrial fibrillation(NVAF) or NVAF associated with silent brain infarction (SBI) and to provide biochemistry evidence to antithrombotic therapy. Methods Plasma LPA/AP levels was examined in blood freshly sampled in 235 cases of NVAF who were not receiving any antithrombotic therapy, 116 cases SBI who were not with NVAF and 120 cases healthy volunteers as control enrolled in the LPA and stroke prevention study. Plasma LPA was assayed by measuring its inorganic phosphorus after separation by chromatograph. Meanwhile, the platelet activation in NVAF or (and) SBI were observed. Results SBI was found in 31.5% of the participants with NVAF, and in 37.6% of the elderly NVAF subjects (age60 years old). LPA/AP levels were significantly increased in NVAF with SBI group((3.78±0.61) μmol/L) compared with controls ((2.66±0.49) μmol/L, 95% CI 3.47-4.21,P = 0.000), NVAF without SBI group ((3.29±0.57) μmol/L, 95 % CI 3.01-3.76, P = 0.008), SBI without NVAF group((3.17±0.54) μmol/L, P=0.004). The platelet activation was significantly higherin NVAF with SBI group, the odds ratio (95% CI) was 21.39(10.17 to 45.02),than those in NVAF without SBI group (P<0.01). Conclusion The plasma LPA/AP levels were significantly elevated in NVAF or NVAF with SBI, NVAF contributes to the risk of SBI. Platelet activation may play an important role in the pathogenesis of thromboembolism in NVAF and the measurement of LPA reflects activation of platelets in vivo and may be a useful marker for the diagnosis of thrombosis or prothrombotic states.Consideration of the role of antiplatelet therapy should be given when choosing antithrombotic therapy to NVAF-associated ischemic stroke.

Effects of lysophosphatidic acid on arrhythmia in acute myocardial infarction rats / 吉林大学学报(医学版)

Objective To observe the effects of lysophosphatidic acid(LPA) on arrhythmia in acute myocardial infarction(AMI) rats.Methods AMI models were prepared by ligating the left coronary branch of rats.60 Wistar rats were divided into 5 groups:sham-operated(SO),AMI,AMI+LPA,AMI+pertussis toxin(PTX) and(AMI+)PTX+LPA.ECG were recorded,HR and VPBs were observed as important indexes.Results Incidence of tachycardia and VPBs of unit time in AMI group were increased compared with sham-operated group(P

The diagnostic value of secretory phospholipase A_2 and lysophosphatic acid for ovarian cancer / 中华检验医学杂志

Objective To explore the diagnostic value of secretory phospholipase A2 (sPLA2) and lysophosphatic acid (LPA) for ovarian cancer and evaluate the correlation of sPLA2 activity and LPA level to the prognosis in the patients with ovarian cancer.Methods ~3H oleic acid labeled E. coli membrane and spectrophotometry were used to detect the original and recurrent ovarian cancer. The motive observation between sPLA2 activity and LPA level was done.At the same time, The sensitivity and specificity for the diagnosis of ovarian cancer were analyzed.Results Comparing the original ovarian cancer group with the ovarian benign tumor group, the difference between sPLA2 activity (24.47 ?5.64 U/L,4.94 ?1.86 U/L) and LPA levelc(6.35 ?2.32 ?mol/L,1.92 ?0.75 ?mol/L) were significantly (P

Yangxue qingnao-containing serum inhibits rat vascular smooth muscle cell proliferation induced by lysophosphatidic acid / 中国病理生理杂志

AIM: To observe the effects of Yangxue qingnao-containing serum on rat vascular smooth muscle cell (VSMC) proliferation induced by lysophosphatidic acid (LPA). METHODS: The [ 3H]-TdR incorporation and mitogen-activated protein kinasc (MAPK) activity were measured in cultured VSMC. End product of lipid peroxidation-MDA levels were also detected. RESULTS: 1?10 -9 ,1?10 -8 and 1?10 -7 mol/L LPA enhanced the cultured VSMC [ 3H]-TdR incorporation, increased MAPK activity and MDA content in a concentration-dependent manner. 5%, 10% and 15% Yangxue qingnao-containing serum concentration-dependently inhibited the increase in VSMC [ 3H]-TdR incorporation, MAPK activity and MDA content induced by LPA. CONCLUSIONS: LPA has a stimulating effect on VSMC proliferation. The LPA-induced intracellular signal transduction may be related to MAPK activity. Yangxue qingnao can efficiently inhibit LPA -induced VSMC proliferation,MAPK activity and lipid peroxidation. [

Relationskip between plasma lysophosphatidic acid concentration and the progression of aortic atherosclerotic lesions in diet induced hyperlipidemic infantile rabbits / 中国介入心脏病学杂志

Objective To investigate the relationship between plasma lysophosphatidic acid(LPA) concentration and progression of aortic atherosclerotic lesions for hyperlipidemic diet fed infantile rabbits.Methods Two-month-old infantile rabbits(0.9-1.1 kg) were randomly assigned to normal diet group(group A,n=6) and hyperlipidemic diet group(group B,n=11).Blood lipid levels,LPA,nitric oxide(NO),malondialdehyde(MDA) and superoxide dismutase(SOD) concentrations were taken regularly.The thoracic aorta was taken from a hypertipidemic diet rabbit for pathological study at certion interval of time.Results Electronic microscope analysis revealed subtle changes of aortic wall during 1-2 weeks of the experiment.Fatty streaks(FS) appeared after 4 weeks of hyperlipidemic diet.The degree of FS increased gradually thereafter.Blood lipid levels increased significantly after 1 week of hyperlipidemic diet.Plasma LPA concentration reached its peak level before the appearance of FS.The NO,MDA and SOD concentrations of group B changed significantly proportional to the development of FS.Conclusion Measuring plasma LPA concentration,combined with serum NO,MDA and SOD concentrations can accurately reflect the formation and progression of FS.

Lysophosphatidic acid (LPA) induces the proliferation of astrocytes in rat via pathway of protein kinase C-? and calcium ion in vitro / 中国病理生理杂志

AIM:To determine if lysophosphatidic acid(LPA)regulates the proliferation of astrocytes(AS)and to approach the mechanism of the process.METHODS:The cerebral AS of the neonatal SD rats were cultured in vitro and divided randomly into control group,PKC excitomotor(PMA)group,LPA group,PKC-? inhibitor(Ro31-8220)group,Ro31-8220+PMA group and Ro31-8220+LPA group.The proliferation of the cells was detected by MTT assay and flow cytometry(FCM).The concentration of intra-cellular calcium ion of the cells([Ca~(2+)]_i)which were labeled with Fura-2/AM was determined by ultraviolet spectrophotometer.The change of PKC-? inside the cells was observed by Western blotting.RESULTS:LPA and PMA stimulated the proliferation of AS,they also enhanced the expression of PKC-? and increased the concentration of [Ca~(2+)]_i.After pretreated with Ro31-8220,the abilities of LPA that mentioned above were decreased.The change of [Ca~(2+)]_i was associated with the diversity of PKC-?.CONCLUSION:LPA promotes the proliferation of AS via the way of PKC-? and Ca2+.