[Effect of oxymatrine on apoptosis of hippocampal neurons by p38/JNK signaling pathway].

To investigate the effect and mechanism of oxymatrine(OMT) on hippocampal neurons apoptosis. Effect of OMT on survival of hippocampal neurons was measured by MTT.Effect of OMT on LPS-induced lactate dehydrogenase(LDH) release rate in hippocampal neurons was measured by biochemical methods. Hoechst 33342 staining was used to observe the apoptotic morphology of hippocampal neurons.The mRNA expression levels of Bax, Bcl-2, and Caspase-3 were detected by Real-time quantitative PCR(RT-qPCR), and the protein expression levels of p38, p-p38, JNK, p-JNK, Bax, Bcl-2 and Caspase-3 were detected by Western blot.The results showed that, hippocampal neurons all grew well after treatment by different doses (0.37-6.0 g•L⁻¹) of OMT for 24 h. Stimulation from LPS increased the release of LDH(P<0.01), improved the JNK and p38 phosphorylation levels(P<0.01), increased the proportion of Bax/Bcl-2 and the expression of Caspase-3(P<0.01), and promoted the apoptosis of hippocampal neurons. OMT pretreatment could significantly reduce the release of LDH induced by LPS stimulation(P<0.05 or P<0.01), reduce the p38 and JNK phosphorylation, decrease the expression of Caspase-3 and Bax/Bcl-2(P<0.01), and diminish the apoptosis of hippocampal neurons.In conclusion, OMT could reduce the LPS-induced phosphorylation of p38 and JNK, down-regulate the Bax/Bcl-2 ratio and expression of Caspase-3, thus inhibiting apoptosis of hippocampal neurons. The mechanism may be associated with p38/JNK signaling pathway.

The role of the TLR4/NF-κB signaling pathway in Aß accumulation in primary hippocampal neurons.

The present study aimed to investigate the role of the Toll-like receptor 4 (TLR4)/nuclear factor κB (NF-κB) signaling pathway in the accumulation of amyloid ß protein (Aß) in primary hippocampal neurons of rats. The purity of these cultured neurons was determined by using immunofluorescence techniques. Lipopolysaccharide (LPS, a TLR4 ligand) or CLI-095 (a TLR4 inhibitor) was used to activate or inhibit TLR4 signaling, respectively. Pyrrolidine dithiocarbamate (PDTC), on the other hand, was used to inhibit NF-κB, a downstream effector of the TLR4 signaling pathway. The contents of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and Aß1-42 in the supernatant were assessed by enzyme-linked immunosorbent assay (ELISA). The mRNA levels of TNF-α, IL-1ß, a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10), ß-site APP cleaving enzyme 1 (BACE-1), Presenilin-1 (PS-1), and ß-amyloid precursor protein (ß-APP) were examined by real-time quantitative PCR (RT-qPCR). The protein levels of ADAM10, BACE-1, PS-1 and ß-APP were examined by Western blotting. Meanwhile, the levels of TLR4 mRNA and protein in hippocampal neurons were tested by RT-qPCR and Western blotting, respectively, after stimulation with Aß1-42 at different concentrations. We observed that the purity of cultured hippocampal neurons after being cultured for 7 days was above 95%. Compared with untreated neurons, LPS-treated neurons showed higher expression levels of TNF-α, IL-1ß, BACE-1, PS-1, ß-APP, and Aß1-42, but a lower expression level of ADAM10. These effects were reversed upon pre-treatment with CLI-095 or PDTC. Furthermore, TLR4 expression was upregulated in the presence of Aß1-42. Taken together, these results provide evidence that elevation in the level of inflammatory cytokines accompanies the activation of TLR4 signaling, and that the consequent downregulation of ADAM10 and upregulation of BACE-1/PS-1 are likely responsible for the accumulation of ß-APP and Aß, which in turn increases TLR4 level to create a positive feedback loop that may constitute the basis for the progression of Alzheimer's disease.

[Involvement of Toll-like receptor 4 in apoptosis of hippocampal neurons through Akt/FoxO3a/Bim signaling pathways].

The present study was to investigate whether Toll-like receptor 4 (TLR4)-mediated Akt/FoxO3a/Bim signaling pathway participated in lipopolysaccharide (LPS)-induced apoptosis in hippocampal neurons. The primarily cultured rat hippocampal neurons were treated with LPS, TLR4 antibody+LPS, and LY294002+LPS, respectively. Cell vitality was assayed by CCK-8. Expressions of p-Akt, Akt, p-FoxO3a, FoxO3a, Bim and active-Caspase-3 of each group were detected by Western blot analysis; the mRNA expression of Bim was detected by real-time quantitative PCR; FoxO3a nuclear translocation was detected by fluorescence microscope. The rate of cell apoptosis was assayed by flow cytometry. The results showed that cell vitality of hippocampal neurons decreased after being treated with LPS in a time-dependent way. Compared with the control group, the expressions of p-Akt and p-FoxO3a decreased significantly, FoxO3a translocated into the nucleus, meanwhile, the expression of Bim and active-Caspase-3, and the apoptotic ratio of hippocampal neurons increased in LPS treated neurons. Pretreatment with TLR4 antibody significantly blocked, while PI3K antagonist LY294002 further strengthened these changes induced by LPS. In conclusion, the present study suggests that Akt/FoxO3a/Bim signaling pathways mediated by TLR4 participate in the apoptotic processes of primarily cultured hippocampal neurons treated with LPS, and the activation of TLR4 causes neuronal apoptosis.

The role of Toll-like receptor 4 on inflammation and Aß formation in cortex astrocytes.

To investigate the role and possible molecular mechanism of astrocytes in inflammation and amyloid ß-protein (Aß) formation, in this research, by using LPS to stimulate cultured rat astrocytes in vitro with or without anti-Toll-like receptor 4 (TLR4) antibody pretreatment, we first detected the TLR4, TNF-α, IL-1ß, ß-amyloid precursor protein (ß-APP) and ß-site APP clearing enzyme 1 (BACE1) mRNA with real-time PCR, and TLR4, NF-κB/P65 protein in cultured astrocytes by Western blot, and then further probed the translocation of NF-κB/P65 using immunofluorescence and the contents of TNF-α, IL-1ß and Aß in culture supernatant through ELISA. We found that all of these indexes increased at different degrees after LPS-stimulation. However, if pretreatment with anti- TLR4 antibody, such stimulating effects of LPS on the nuclear translocation of NF-κB/P65 and TNF-α, IL-1ß, Aß contents in astrocytic culture supernatant were reduced significantly or disappeared in comparison with the group with only LPS-administration. Our results suggest that TLR4 in astrocytes might play an important role in the inflammation and Aß formation through the TLR4/NF-κB signaling pathway, thus providing new knowledge and understanding of the inflammatory hypothesis of AD pathogenesis.

Amelioration of glomerulosclerosis with all-trans retinoic acid is linked to decreased plasminogen activator inhibitor-1 and α-smooth muscle actin.

AIM: To examine the effects of all-trans retinoic acid (atRA) on renal morphology and function as well as on renal plasminogen activator inhibitor-1 (PAI-1) expression and plasmin activity in rats with 5/6 nephrectomy. METHODS: Adult male Sprague Dawley rats were given 5/6 nephrectomy or sham operation. Renal function was measured 2 weeks later. The nephrectomized rats were assigned to groups matched for proteinuria and treated with vehicle or atRA (5 or 10 mg/kg by gastric gavage once daily) for the next 12 weeks. Rats with sham operation were treated with vehicle. At the end of the treatments, kidneys were collected for histological examination, Western blot analysis, and enzymatic activity measurements. RESULTS: The 5/6 nephrectomy promoted hypertension, renal dysfunction, and glomerulosclerosis. These changes were significantly reduced in the atRA-treated group. The expressions of PAI-1 and α-smooth muscle actin (α-SMA) were significantly increased in the vehicle-treated nephrectomized rats. Treatment with atRA significantly reduced the expressions of PAI-1 and α-SMA. However, plasmin activity remained unchanged following atRA treatment. CONCLUSION: Treatment with atRA ameliorates glomerulosclerosis and improves renal function in rats with 5/6 nephrectomy. This is associated with a decrease in PAI-1 and α-SMA, but not with a change in plasmin activity.

Ginseng for cognition.

BACKGROUND: Ginseng is a herbal medicine in widespread use throughout the world. Its effect on the brain and nervous system has been investigated. It has been suggested, on the basis of both laboratory and clinical studies, that it may have beneficial effects on cognitive performance. OBJECTIVES: To evaluate the efficacy and adverse effects of ginseng given to improve cognitive performance in healthy participants, participants with cognitive impairment or dementia.To highlight the quality and quantity of research evidence available. SEARCH STRATEGY: The Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (CDCIG), The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS, clinical trials registries and grey literature sources were searched on 24 February 2009 using the following terms: ginseng* OR panax OR ginsan OR "Jen Shen"OR shinseng OR Renshen OR schinseng OR ninjin OR gingilone OR panaxoside* OR ginsenoside* OR protopanaxa* OR protopanaxadiol OR protopanaxatriol OR panaxagin OR ginsenol OR ginsenine and terms for dementia and cognition. The CDCIG Specialized Register contains records from all major health care databases (The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS) as well as from many clinical trials registries and grey literature sources. SELECTION CRITERIA: All double-blind and single-blind randomized, placebo controlled trials assessing the effects of ginseng on cognitive function were eligible for inclusion. Interventions were considered to be ginseng if they were compounds containing ginseng or active agents of the Panax genus as the major component. DATA COLLECTION AND ANALYSIS: Characteristics of each included trial were extracted independently by two reviewers using a self-developed data extraction form and entered into RevMan 5.0 software. Authors of identified trials were contacted for additional information and unpublished data. The effects of ginseng in healthy participants, participants with cognitive impairment or dementia were addressed independently. MAIN RESULTS: Nine randomized, double-blind, placebo controlled trials meeting the inclusion criteria were identified. Eight trials enrolled healthy participants, and one was of subjects with age-associated memory impairment (AAMI).Only five of the identified trials had extractable information and were included in the analysis. Four studies investigated the effects of ginseng extract and one assessed the efficacy of ginseng compound HT008-1. All of these trials investigated the effects of ginseng on healthy participants. Pooling the data was impossible owing to heterogeneity in outcome measures, trial duration, and ginseng dosage. Results of the analysis suggested improvement of some aspects of cognitive function, behavior and quality of life. No serious adverse events associated with ginseng were found. AUTHORS' CONCLUSIONS: Currently, there is a lack of convincing evidence to show a cognitive enhancing effect of Panax ginseng in healthy participants and no high quality evidence about its efficacy in patients with dementia. Randomized, double-blind, placebo-controlled, parallel group trials with large sample sizes are needed to further investigate the effect of ginseng on cognition in different populations, including dementia patients.

[Effects of Chinese herb compound Naoyikang on expression of choline acetyltransferase in brain of rats with Alzheimer's disease].

OBJECTIVE: To observe the effects of Naoyikang (NYK) on expression of choline acetyltransferase (ChAT) in brain of rats with Alzheimer' s disease (AD). METHOD: Bilateral infusions of Ibotenic acid (IBO) into nucleus basalis of Meynert (NBM) using hamilton syringe and stereotaxic apparatus were adopted to establish the rat model of AD. After intragastrically administrated with different solution for 28 days, immunohistochemistry and Western-blot were adopted to study the expression of ChAT in frontal cortex of AD rats. RESULT: NYK could improve the morphology and increase the number of ChAT immunoreactive neurons, and significantly promote ChAT protein expression. CONCLUSION: NYK may be able to increase the synthesis of acetylcholine (ACh) through elevating the expression of ChAT protein, thus improving the level of brain ACh so as to protect central cholinergic neurons.

[Inhibitory effects of anisodamine and pentoxifylline on the expression of lipopolysaccharide -induced intercellular adhesion molecule-1 in rat cardiac muscle].

OBJECTIVE: To investigate the inhibitory effects of anisodamine (654-2) and pentoxifylline (PTX) on the expression of lipopolysaccharide (LPS)-induced intercellular adhesion molecule-1 (ICAM-1) in rat cardiac muscle in vivo. METHODS: The animals were randomly divided into five groups (each n=6): (1) normal control group, (2) model group, (3) 654-2 treated group, (4) PTX treated group and (5) 654-2+PTX treated group. The endotoxemia model was reproduced by intravenous injection LPS 5 mg/kg. The expression of ICAM-1 protein in rat cardiac muscle was assayed by Western blotting at 0, 2, 4, 6, 8, 10 hours after intravenous LPS injection. Then the expression of ICAM-1 protein in different groups was assayed at different time points. RESULTS: The changes in expression of ICAM-1 in rat cardiac muscle after LPS injection were in a time-dependent pattern, gradually elevating to approach the peak at 6 th, then it lowered, but it still appeared at 10 hours (P<0.05). Western blotting also showed that ICAM-1 protein with decreased with pre-treatment of 654-2 or PTX respectively (both P<0.01). It was reduced to a much lower level when the animals were pretreated with a combination of 654-2 and PTX, compared with the group of 654-2 alone or PTX alone (both P<0.05). CONCLUSION: The combination of 654-2 and PTX may play a protective role in rat against injury to cardiac muscle induced by LPS in vivo via inhibiting the production of ICAM-1 protein.

Inhibitory effect of oxymatrine on hepatocyte apoptosis via TLR4/PI3K/Akt/GSK-3ß signaling pathway.

AIM: To evaluate the effect of oxymatrine (OMT) on hepatocyte apoptosis in rats with lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced acute liver failure (ALF). METHODS: LPS/D-GalN was used to establish a model of ALF in rats. To evaluate the effect of OMT, we assessed apoptosis by transmission electron microscopy, and the pathological changes in the liver by light microscopy with hematoxylin and eosin staining. An automated biochemical analyzer was used to measure serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Enzyme-linked immunosorbent assay was used to determine the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1ß. Western blotting was used to detect protein levels in liver tissues. Streptavidin peroxidase immunohistochemistry was used to observe expression of Toll-like receptor (TLR)4, active caspase-3, Bax and Bcl-2. RESULTS: All rats in the normal control and OMT-pretreated groups survived. The mortality rate in the model group was 30%. OMT preconditioning down-regulated apoptosis of hepatocytes and ameliorated pathological changes in liver tissue. The levels of AST, ALT, TNF-α and IL-1ß in the model group increased significantly, and were significantly reduced by OMT pretreatment. OMT pretreatment down-regulated expression of TLR4 and active caspase-3 and the Bax/Bcl-2 ratio, and up-regulated expression of P-AktSer473 (Akt phosphorylated at serine 473) and P-GSK3ßSer9 (glycogen synthase kinase 3ß phosphorylated at serine 9) induced by LPS/D-GalN. CONCLUSION: OMT inhibits hepatocyte apoptosis by suppressing the TLR4/PI3K/Akt/GSK-3ß signaling pathway, which suggests that OMT is an effective candidate for ameliorating acute liver failure.

[The role of TLR4/P38/JNK signaling pathway in apoptosis of hippocampal neurons].

OBJECTIVE: To investigate the effects of the Toll like receptor 4 (TLR4) -P38-JNK signaling pathway in the apoptosis of hippocampal neurons in rats and its mechanisms. And to provide new experimental evidences for the pathogenesis research, prevention and treatment of neurodegenerative diseases (ND). METHODS: The hippocampal neurons derived from newborn rat were cultured for 7 d in vitro. The purity of hippocampal neurons was identified by immunofluorescence method. In order to activate or block the action of TLR4, the hippocampal neurons were pretreated with TLR4 ligand lipopolysaccharide (LPS) or TLR4 antibody. In the experiment 1, the hippocampal neurons were divided into normal control group, LPS group and TLR4 antibody+LPS group. The expressions of P-P38 and P-JNK were deteced by immunofluorescence. In the experiment 2, the hippocampal neurons were divided into 6 groups:normal control group, LPS group, TLR4 antibody +LPS group, SB202190(inhibitor P38)+LPS group, SP600125(inhibitor JNK)+LPS group, PD98059(inhibitor ERK)+LPS group. The cells in above mentioned groups were pretreated with TLR4 antibody, the inhibitors of P38, JNK or ERK for 2 h respectively. Then, all the six groups were stimulated by LPS for 24 h. The expressions of Bcl-2, Bax and Active-caspase-3 were detected by Western blot. The hippocampal neuronal apoptosis rate were tested with flow cytometry. RESULTS: The expressions of P-P38 and P-JNK of hippocampal neurons in LPS group were higher than those in normal control group (P<0.01). Compared with LPS group, the expressions of P-P38 and P-JNK were decreased significantly in TLR4 antibody +LPS group (P<0.01). Compared with the normal control group, the expressions of Bcl-2/Bax were decreased, while the expression of Active-caspase-3 was increased in the hippocampal neurons after LPS stimulation (P<0.01). The apoptotic rate of hippocampal neurons was higher in LPS group than that in the control group (P<0.01). Compared with LPS group, the expressions of Bcl-2/Bax were increasd and the expression of Active-caspase-3 was decreased in TLR4 antibody+LPS group, SB202190+LPS group, and SP600125+LPS group. The apoptotic rate of hippocampal neurons was significantly lower than that in the LPS group (P<0.05, P<0.01). The cell apoptosis rate had no significant differences between PD98059+LPS group and LPS group. CONCLUSIONS: ①TLR4-mediated P38/JNK signaling pathway exists in hippocampal neurons. ②After TLR4 activation in hippocampal neurons, the expressions of P-P38 and P-JNK are up-regulated, the expressions of Bcl-2/Bax are decreased and the expression of Active-caspase-3 is increased, which promote apoptosis of hippocampal neurons. TLR4/P38/JNK signaling pathway is involved in apoptosis of hippocampal neurons.

Total Laparoscopic Hysterectomy in Patients with Large Uteri: Comparison of Uterine Removal by Transvaginal and Uterine Morcellation Approaches.

The aim of this study was to compare the clinical results of total laparoscopic hysterectomy (TLH) for large uterus with uterus size of 12 gestational weeks (g.w.) or greater through transvaginal or uterine morcellation approaches. We retrospectively collected the clinical data of those undergoing total laparoscopic hysterectomies between January 2004 and June 2012. Intraoperative and postoperative outcomes were compared between patients whose large uterus was removed through transvaginal or morcellation approaches. The morcellation group has significantly shorter mean operation time and uterus removal time and smaller incidence of intraoperative complications than the transvaginal group (all P < 0.05). No statistical significant difference regarding the mean blood loss, uterine weight, and length of hospital stay was noted in the morcellation and transvaginal groups (all P > 0.05). In two groups, there was one patient in each group who underwent conversion to laparotomy due to huge uterus size. With regard to postoperative complications, there was no statistical significant difference regarding the frequencies of pelvic hematoma, vaginal stump infection, and lower limb venous thrombosis in two groups (all P > 0.05). TLH through uterine morcellation can reduce the operation time, uterus removal time, and the intraoperative complications and provide comparable postoperative outcomes compared to that through the transvaginal approaches.

[The role of TLR4-mediated MyD88-dependent pathway in neuroinflammation in hippocampal neurons of rats].

OBJECTIVE: To investigate weather there is a toll-like receptor 4 (TLR4)-mediated myeloid differentiation factor 88 (MyD88)-dependent pathway in hippocampal neurons of rats and the probable role of the pathway in neuroinflammation. METHODS: To establish the proper model, primarily cultured hippocampal neurons were treated with lipopolysaccharides (LPS), or pretreated with TLR4 antibody then co-treated with LPS. The expression of mRNA of MyD88 and TNF-alpha receptor associated factor 6 (TRAF6) were tested by RT-qPCR. The content of MyD88 and TRAF6 were tested by Western blot. The nuclear translocation of nuclear factor-kappaB/P65 (NF-kappaB/p65) was tested by immunofluorescence. The content of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and nitric oxide (NO) were tested by ELISA. RESULTS: LPS could increase MyD88 and TRAF6 mRNA, upregulate protein level of MyD88 and TRAF6 and increase the level of TNF-alpha, IL-1beta and NO in cell culture supernatant. LPS also could promote NF-kappa B/p65 translation to the nucleus. The pretreatment with TLR4 antibody reduced the translocation to nucleus for NF-kappaB/P65 and the contents of TNF-alpha, IL-1beta and NO in the culture supernatant. CONCLUSION: There is a TLR4-mediated MyD88-dependent pathway in hippocampal neurons. The activation of this pathway can increase the level of TNF-alpha, IL-1beta and NO in cell culture supernatant. TLR4-mediated MyD88-dependent pathway in hippocampal neurons participate in neuroinflammation, that means neurons are not passive in inflammation.

[The effect of meloxicam on the inflammatory reaction induced by beta amyloid protein in Alzheimer's disease rats].

OBJECTIVE: To investigate the effect and mechanism of meloxicam on the inflammatory reaction induced by beta amyloid protein (AB) in Alzheimer's disease (AD) rats. METHODS: The rat model was established by microinjection of Abeta(1-40) into hippocampus. The expression of NF-kappaB p65 and glial fibrillary acidic protein (GFAP) in hippocampus were detected by immunohistochemistry. The content of GFAP in cortex was tested by Western-blot. The content of TNF-alpha in cortex was tested by ELISA. The expression of IL-1beta mRNA was tested by RT-PCR. RESULTS: The expression of NF-kappaB p65, GFAP and TNF-alpha as well as IL-1beta mRNA were decreased by meloxicam. CONCLUSION: Meloxicam can reduce the proliferation of astrocyte by decreasing the expression of GFAP in AD model rat's hippocampus and cortex. And the depression of NF-kappaB p65 may significantly decrease the expression of TNF-alpha1 and IL-1beta to lessen the inflammatory reaction in cerebral tissue.

[Protective effect of Naoyikang on the Alzheimer's disease model mice induced by D-galactose and NaNO2].

AIM: To investigate the mechanisms of Naoyikang (Traditional Chinese Medicine) on the Alzheimer's Disease (AD) model mice induced by D-galactose (D-gal) and NaNO2. METHODS: The mouse model was established by intraperitoneal injection of D-gal and NaNO2. The capacity of learning and memory was tested on mice with electrical maze; the content of nitric oxide (NO) and the activity of monoamine oxidase-B (MAO-B), glutathione peroxidase (GSH-PX), Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme in cerebral cortex and hippocampus were assayed by biochemical methods; expression of Bax and Bcl-2 mRNA was detested by RT-PCR. RESULTS: Naoyikang could ameliorate the capacity of learning and memory of AD model mice and reduce MAO-B activity in the brain tissue and activate the activity of Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme in the brain tissue and decrease the expression of Bax mRNA, but increase the expression of Bcl-2 mRNA in the model brain tissue. CONCLUSION: Naoyikang could protect AD model mice induced by D-gal and NaNO2. It could modify the metabolism of monoamine neurotransmitter in brain through reducing MAO-B activity and protect neurons by activating the activity of Na(+) -K(+) -ATP enzyme and Ca(2+) -ATP enzyme and decrease Bax expression and increase Bcl-2 expression in the model brain tissue.

[Effect of acupoint-injection of oxymatrine on experimental hepatic carcinoma and study on the mechanism].

OBJECTIVE: To investigate the effect of acupoint injection of oxymatrine (OM) on experimental hepatocellular carcinoma and the mechanism. METHODS: The rats of hepatocellular carcinoma induced by 2-acetoaminoflurence (2-AAF) were randomly divided into a normal control group (group N), a model group (group M), a control group of oxymatrine intraperitoneal injection (OM ip group) and a treatment group of small dose oxymatrine injection into Zusanli (OM ZSL group). At the end of 12h week, the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (gamma-GT) were determined. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expressions of cyclin D1 and cyclin-dependent kinase 4 (CDK4) mRNA in hepatocellular carcinoma tissues. RESULTS: The number of cancer nodes on the surface of liver in th Om ip group and the Om ZSL group was lower than in the group M, with the serum ALT, AST, and gamma-GT levels significantly decreased (P<0. 01), and significantly inhibited expressions of cyclin D1, CDK4 mRNA (P<0. 01). CONCLUSION: OM ip and small dose oxymatrine injection into ZSL can treat or delay hepatocarcinogenisis of hepatocellular carcinoma induced by 2-AAF. Partial mechanism of this anti-carcinoma is protecting hepatocytes possibly through improving hepatic functions, and inhibiting excessive proliferation of liver cancer cells via inhibiting the expressions of cyclin Dl, CDK4 mRNA.

[Protective effect of Naoyikang on the damage induced by glutamate in hippocampal neuron].

AIM: To investigate the effect of Naoyikang serum on the damage induced by glutamate in hippocampal neuron. METHODS: Morphological observation, MTT assay and nuclear DNA-associated fluorescence with DAPI dye were applied to evaluate the viability of hippocampal neuron, immunocytochemistry and RT-PCR were used to determine the expression of PTEN. RESULTS: A decreased viability and increased expression of PTEN were shown in hippocampal neuron in response to the treatment with glutamate. It was shown that the percentage of cell death and the expression of PTEN were reduced by the treatment with Naoyikang serum. CONCLUSION: These results suggest that Naoyikang may prevent the toxicity of glutamate by suppressing the expression of PTEN.

[Advances in the chiral resolution of organophosphorus compounds by liquid chromatography].

The developments in the chiral resolution of organophosphorus compounds by liquid chromatography in recent years are reviewed. Two different approaches of separation: indirect resolution (chiral derivatization reagent method) and direct resolution (chiral mobile phase additive and chiral stationary phase), focusing on several chiral stationary phases--Pirkle type, cyclodextrin, cellulose, ligand exchange and other chiral stationary phases are presented. The possible mechanism of chiral recognition is discussed. Eighty-five references are involved.