Identification of compound mutations of SLC12A3 gene in a Chinese pedigree with Gitelman syndrome exhibiting Bartter syndrome-liked phenotypes.

BACKGROUND: Gitelman syndrome is a rare salt-losing renal tubular disorder associated with mutation of SLC12A3 gene, which encodes the Na-Cl co-transporter (NCCT). Gitelman syndrome is characterized by hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria, and renin-angiotensin-aldosterone system (RAAS) activation. Different SLC12A3 variants may lead to phenotypic variability and severity. METHODS: In this study, we reported the clinical features and genetic analysis of a Chinese pedigree diagnosed with Gitelman syndrome. RESULTS: The proband exhibited hypokalaemia, hypomagnesemia, metabolic alkalosis, but hypercalciuria and kidney stone formation. The increased urinary calcium excretion made it confused to Bartter syndrome. The persistent renal potassium wasting resulted in renal tubular lesions, and might affect urinary calcium reabsorption and excretion. Genetic analysis revealed mutations of SLC12A3 gene with c.433C > T (p.Arg145Cys), c.1077C > G (p.Asn359Lys), and c.1666C > T (p.Pro556Ser). Potential alterations of structure and function of NCCT protein due to those genetic variations of SLC12A3 are predicted. Interestingly, one sibling of the proband carried the same mutant sites and exhibited similar clinical features with milder phenotypes of hypokalemia and hypomagnesemia, but hypocalciuria rather than hypercalciuria. Family members with at least one wild type copy of SLC12A3 had normal biochemistry. With administration of spironolactone, potassium chloride and magnesium supplement, the serum potassium and magnesium were maintained within normal ranges. CONCLUSIONS: In this study, we identified compound mutations of SLC12A3 associated with varieties of clinical features. Further efforts are needed to investigate the diversity in clinical manifestations of Gitelman syndrome and its correlation with specific SLC12A3 mutations.

Glycyrrhizic acid ammonium salt alleviates Concanavalin A-induced immunological liver injury in mice through the regulation of the balance of immune cells and the inhibition of hepatocyte apoptosis.

Glycyrrhizic acid ammonium salt (GAAS) is derived from glycyrrhizic acid, which is an active compound extracted from the Chinese traditional medicine licorice. GAAS is clinically applied to treat immune-mediated liver injury, but its mechanism remains elusive. Therefore, this study aimed to investigate the mechanism in which GAAS alleviates immune-mediated liver injury induced by Concanavalin A (ConA). After ten days of intragastric administration of GAAS, 20 mg/kg ConA was injected via tail vein to establish the immune-mediated liver injury model of BALB/C mice. Then, the concentrations of ALT, AST, and TBIL in the serum of mice were determined. H&E staining was performed to observe the pathological changes in the liver, and the expression of liver cytokines was detected by qPCR. Immunohistochemistry and Western blot analysis was employed to detect the expression of liver-related proteins. The apoptosis in liver tissue was detected by TUNEL. Our results suggest that GAAS demonstrated excellent protective effects in the liver. We found that GAAS down-regulated the mRNA expression of IL-1ß, IL-6, TNF-α, IFN-γ, and IL-17A, and it up-regulated the mRNA expression of IL-4 and TGF-ß. Additionally, GAAS may modulate the balance of four immune cells (Th1, Th2, Th17, and Treg) by regulating the expression of T-bet, GATA3, RORγt, and Foxp3 to alleviate liver injury in mice. Furthermore, GAAS decreased hepatocyte apoptosis by blocking the JAK1/STAT1/IRF1 pathway, suppressing oxidative stress, decreasing p-JNK expression, and regulating the expression of apoptosis-related proteins. In summary, the mechanism of GAAS in liver injury alleviation acts to regulate the balance of Th cells in the liver to inhibit hepatocyte apoptosis. This study may provide a new strategy for the treatment of immune-mediated liver injury.

Elevated Prevalence of Abnormal Glucose Metabolism and Other Endocrine Disorders in Patients with ß-Thalassemia Major: A Meta-Analysis.

BACKGROUND: Endocrinopathies are common in patients with ß-thalassemia major despite parenteral iron chelation therapy with deferoxamine. Prevalence of abnormal glucose metabolism in previous studies was controversial. The aim of this study was to discuss the prevalence of abnormal glucose metabolism in ß-thalassemia major based on a meta-analysis. METHODS: PubMed, ScienceDirect, Springerlink, Ovid, Web of Science, MEDLINE, Wanfang database, and Chinese National Knowledge Internet were searched for relevant articles. Two authors selected the articles according to the inclusion criteria and then extracted the data. The prevalence of diabetes mellitus (DM) in ß-thalassemia major was defined as the primary outcome. The prevalence with the 95% confidence interval (95%CI) was used to evaluate the proportion of abnormal glucose metabolism and other endocrine disorders in patients with ß-thalassemia major. Subgroup analyses were applied to explore the prevalence in different regions. Sensitivity analysis and publication bias assessment were also conducted. RESULTS: A total of 44 studies with 16605 cases were included in this analysis. Diabetes mellitus was present in 6.54% (95% CI: 5.30%-7.78%). The fixed subgroup study revealed that the region with the highest prevalence was the Middle East (prevalence= 7.90%, 95% CI: 5.75%-10.05%). The accumulated meta-analysis revealed that the prevalence of DM in ß-thalassemia major was relatively steady in each year. The prevalence of impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and other endocrine disorders in ß-thalassemia major was 17.21% (95% CI: 8.43%-26.00%), 12.46% (95% CI: 5.98%-18.94%), and 43.92% (95% CI: 37.94%-49.89%), respectively. Sensitivity analysis showed that the pooled results were robust; publication bias assessment revealed that there was no significant evidence that the pooled results were influenced by publication bias. CONCLUSION: High prevalence of endocrine disorders involving abnormal glucose metabolism was detected in ß-thalassemia major. Treatment and prevention measurements may be necessary to prevent growth and endocrine problems.

Hydroxysafflor Yellow A Inhibits TNF-α-Induced Inflammation of Human Fetal Lung Fibroblasts via NF-κB Signaling Pathway.

OBJECTIVE: Hydroxysafflor yellow A (HSYA), an effective ingredient of the Chinese herb Carthamus tinctorius L, attenuated bleomycin-induced pulmonary fibrosis in mice. This study is to investigate the effect of HSYA on the proliferation and inflammatory level of human fetal lung fibroblasts (MRC-5 cells) induced by tumor necrosis factor-α (TNF-α) and explore the underlying mechanisms. METHODS: MRC-5 cells were treated with different concentrations of TNF-α, HSYA, or/and etanercept (ENCP, TNF-α receptor (TNFR1) antagonist, 500 ng/mL) before cell proliferation was detected. The laser confocal microscope was used to observe the role of HSYA in binding of TNF-α and its receptor. Co-immunoprecipitation was used to detect the binding of TNFR1 and TAK1-TAB2 complex. Real-time quantitative RT-PCR and western blot were used to detect the expressions of inflammation-related cytokines and proteins related with the NF-κB pathway. Luciferase reporter gene assay and chromatin coprecipitation method were used to detect the interaction between AP-1 and TGF-ß1 promoter. RESULTS: TNF-α (5 ng/mL) was used to induce inflammation and proliferation in MRC-5 cells. HSYA can partially suppress the stimulation of TNF-α on proliferation and inflammatory response of MRC-5 cells. HSYA could compete with TNF-α to bind with TNFR1 and hamper the binding of TNFR1 to TAK1-TAB2 complex. In addition, HSYA could also inhibit the activation of the NF-κB signal pathway and suppress the binding of TGF-ß1 promoter with AP-1. CONCLUSION: Evidence in this study suggested that HSYA affects TNF-α-induced proliferation and inflammatory response of MRC-5 cells through the NF-κB/AP-1 signaling pathway, which may provide theoretical basis for HSYA treatment in pulmonary fibrosis.

Active saponins from root of Pueraria peduncularis (Grah. ex Benth.) Benth. and their molluscicidal effects on Pomacea canaliculata.

BACKGROUND: Pueraria peduncularis (Grah. ex Benth.) Benth., which belongs to the Leguminosae family, exhibits resistance to many crop pests in agricultural production. Pomacea canaliculata is an important invasive snail in rice fields and causes severe yield losses. To evaluate the toxicity of P. peduncularis to P. canaliculata, in this study the molluscicidal activity of root extracts of P. peduncularis was tested against P. canaliculata; the active compounds were isolated, and the structures of these compounds were analysed using nuclear magnetic resonance (NMR) analysis and mass spectral analysis. RESULTS: Our results showed that the molluscicidal activity of the root crude extract differed between P. canaliculata with different shell diameters after treatment for 72 h. The median lethal concentration (LC50 ) was 5.511 mg L-1 against snails of 1.5 ± 0.2 cm diameter and 12.383 mg L-1 against snails of 2.5 ± 0.2 cm diameter. Furthermore, two active ingredients isolated from root methanol extracts were identified as pedunsaponin A and pedunsaponin C. Both pedunsaponin A and pedunsaponin C showed strong molluscicidal activities, with LC50 values of 3.893 and 4.252 mg L-1 , respectively, against snails with shell diameters of 1.5 ± 0.2 cm after treatment for 72 h. CONCLUSION: Pueraria peduncularis extracts exhibit high molluscicidal activity and have great potential value for exploring a molluscicide to control Pomacea canaliculata. © 2016 Society of Chemical Industry.

Effects of Maternal Chromium Restriction on the Long-Term Programming in MAPK Signaling Pathway of Lipid Metabolism in Mice.

It is now broadly accepted that the nutritional environment in early life is a key factor in susceptibility to metabolic diseases. In this study, we evaluated the effects of maternal chromium restriction in vivo on the modulation of lipid metabolism and the mechanisms involved in this process. Sixteen pregnant C57BL mice were randomly divided into two dietary treatments: a control (C) diet group and a low chromium (L) diet group. The diet treatment was maintained through gestation and lactation period. After weaning, some of the pups continued with either the control diet or low chromium diet (CC or LL), whereas other pups switched to another diet (CL or LC). At 32 weeks of age, serum lipid metabolism, proinflammatory indexes, oxidative stress and anti-oxidant markers, and DNA methylation status in adipose tissue were measured. The results indicated that the maternal low chromium diet increased body weight, fat pad weight, serum triglyceride (TG), low-density lipoprotein cholesterol (LDL), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), and oxidized glutathione (GSSG). There was a decrease in serum reduced/oxidized glutathione (GSH/GSSG) ratio at 32 weeks of age in female offspring. From adipose tissue, we identified 1214 individual hypomethylated CpG sites and 411 individual hypermethylated CpG sites in the LC group when compared to the CC group. Pathway analysis of the differential methylation genes revealed a significant increase in hypomethylated genes in the mitogen-activated protein kinase (MAPK) signaling pathway in the LC group. Our study highlights the importance of the MAPK signaling pathway in epigenetic changes involved in the lipid metabolism of the offspring from chromium-restricted dams.

Chuanhu anti-gout mixture versus colchicine for acute gouty arthritis: a randomized, double-blind, double-dummy, non-inferiority trial.

BACKGROUND: The Chuanhu anti-gout mixture has been used for many years in the treatment of gout in Chinese Traditional Medicine, and current methods for treatments for acute gouty arthritis have been either less effective or have had serious side effects. METHODS: In this 12-week, double-blind, double-dummy, non-inferiority study, outpatient individuals with newly diagnosed acute gouty arthritis were randomly assigned to receive Chuanhu anti-gout mixture or colchicine. Both the study investigators and the participants were masked to the treatment assignments. The primary outcome was the recurrence rate of acute gouty arthritis, and the secondary outcomes were changes in white blood cells (WHC) and C-reactive protein (CRP). This trial is registered at ISRCTN.org as trial ISRCTN65219941. RESULTS: A total of 176 patients were randomly assigned to receive either the Chuanhu anti-gout mixture or Colchicine. The overall recurrence rates in the Chuanhu anti-gout mixture group (CH group) and the Colchicine group (Col group) were 12.50% vs 14.77% (difference -2.22%, 95% confidence interval (95% CI): -10.78%~6.23%), meeting the predefined non-inferiority criterion of 15%, as did the data for WHC and CRP. The incidence of adverse events (mainly diarrhea) was less in the Col group than in the CH group (2.27% vs 28.41%, 95% CI 0.01~0.26). In addition, changes in blood uric acid, alanine aminotransferase, aspartate aminotransferase and creatinine in the CH group were significantly larger compared to those in the Col group (P<0.05). CONCLUSIONS: The Chuanhu anti-gout mixture was non-inferior to colchicine for the treatment of acute gouty arthritis. The study suggested that the Chuanhu anti-gout mixture can be considered an alternative choice for the treatment of acute gouty arthritis because of its lower incidence of adverse events and its protection of kidney and renal function.

Attenuating effect of Fufang Xueshuantong Capsule on kidney function in diabetic nephropathy model.

Fufang Xueshuantong Capsule (FXST) can reduce urinary albumin and whole blood viscosity in early diabetic nephropathy (DN) patients. This research aimed to investigate the effect of FXST on kidney function in DN rats and to identify the underlying molecular mechanisms. We performed Illumina RatRef-12 Expression BeadChip gene array analysis, and found that 3-month treatment with FXST significantly decreased 24-h urinary albumin, serum creatinine and blood urea nitrogen, and increased urinary creatinine in DN model rats. Kidney hypertrophy and glomerular mesangial matrix expansion were also ameliorated. Kidneys from the high-dose FXST group had 67 genes with significantly changed expression (34 increased, 33 decreased). DAVID analysis showed that the fold enrichment score of "collagen type 1" was the highest in all GO functional categories. DAVID function annotation cluster analysis indicated that the top annotation cluster included three GO function categories: "response to nutrient", "response to nutrient levels" and "response to extracellular stimulus". Based on KEGG pathway analysis, we found that the most two significant pathways were "metabolism of xenobiotics by cytochrome P450" and "drug metabolism". Real-time PCR showed that relative levels of Col1a1 (collagen type 1 alpha 1), Ctgf (connective tissue growth factor) and Tgfb1 (transforming growth factor beta 1) were significantly decreased in the FXST group, while Cyp2c23 (cytochrome P-450 family 2 subfamily C polypeptide 23) and Nphs1 (nephrin) were increased. The increased expressions of TGFß and collagen (type 1, α2) in the kidneys of DN rats were attenuated by FXST. Our data suggest that FXST can moderate kidney function in DN rats. The mechanism may involve the BMP2-TGFß-CTGF pathway, CYP2C23 and podocyte proteins.

[Effect of zedoary oil for cat D and cat K expression in A549 cell line].

OBJECTIVE: To explore the Zedoary oil on A549 cell line of collagen deposition cat D and cat K expression. METHOD: The A549 cell line were treat by Zedoary oil on four different concentrations (0, 40, 80, 120 mg x L(-1)) in different time. Dynamic changes of collagen in A549 cell using Picric-sirius red method. Cat D and Cat K expression of level were detected by using western blot. RESULT: The collagen content showed that Zedoary oil had an inhibitory effect on the deposition of A549 cells. The results of western blot showed that the expression of cat D and cat K were up-regulated significangly in A549 cells of Zedoary oil groups compared with that in controls. CONCLUSION: A549 cell of collagen deposition were reduced by Zedoary oil. The effects may due to the up-regulation of cat D and cat K.

In silico and in vitro analyses identified three amino acid residues critical to the catalysis of two aphid farnesyl diphosphate synthase.

Farnesyl diphosphate synthase (FPPS) plays an essential role in the isoprenoid biosynthetic pathway of microbes, plants and animals. In the present study, we first cloned two FPPSs from the bird cherry-oat aphid (RpFPPS1 and RpFPPS2), and activity assay by gas chromatography-mass spectrometry showed that both RpFPPS1 and RpFPPS2 were active in vitro. They were then subjected to homology modeling and molecular docking. Molecular interaction analysis indicated that three amino acid residues (R120, R121 and K266) might play key roles in the catalysis of the two aphid FPPSs by forming hydrogen bonds with the diphosphate moiety of the allylic substrate. These in silico results were subsequently confirmed by site-directed mutagenesis and in vitro activity assay of the mutant enzymes, in which each of the single mutations R120G, R121G and K266I abolished the activities of the two FPPSs. This study contributes to our understanding of the catalytic mechanism of farnesyl diphosphate synthases.

Telmisartan improves kidney function through inhibition of the oxidative phosphorylation pathway in diabetic rats.

Telmisartan provides renal benefit at all stages of the renal continuum in patients with type 2 diabetes mellitus. This research is to investigate the effect of telmisartan on kidney function in diabetic rats and to identify the underlying molecular mechanisms. Diabetic rats were divided into vehicle group, low dosage (TeL) group, and high dosage of telmisartan (TeH) group. We performed Illumina RatRef-12 Expression BeadChip gene array experiments. We found 3-months of treatment with telmisartan significantly decreased 24-h urinary albumin, serum creatinine, blood urea nitrogen, and increased creatinine clearance rate. Kidney hypertrophy and glomerular mesangial matrix expansion were ameliorated. The glomeruli from the TeH group had 1541 genes with significantly changed expression (554 increased, 987 decreased). DAVID (Database for annotation, visualization and Integrated discovery) analyses showed that the most enriched term was 'mitochondrion' (Gene Ontology (GO:0005739)) in all 67 GO functional categories. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses indicated that all differentially expressed genes included seven KEGG pathways. Of those pathways, four are closely related to the oxidative phosphorylation pathway. Quantitative real-time PCR verified that the H+ transporting mitochondrial F1 complex, beta subunit (Atp5b), cytochrome c oxidase subunit VIc (Cox6c), and NADH dehydrogenase (ubiquinone) Fe-S protein 3 (Ndufs3) were significantly downregulated both in TeL and TeH groups, while nephrosis 1 homolog (Nphs1) and nephrosis 2 homolog (Nphs2) were significantly upregulated. The increased expression of malonaldehyde and NDUFS3 in the glomeruli of diabetic rats was attenuated by telmisartan. The other significantly changed pathway we found was the peroxisome proliferator-activated receptor (PPAR) signaling pathway. Our data suggest that telmisartan can improve kidney function in diabetic rats. The mechanism may be involved in mitochondrion oxidative phosphorylation, the PPAR-γ pathway, and the slit diaphragm.

Berberine Moderates Glucose and Lipid Metabolism through Multipathway Mechanism.

Berberine is known to improve glucose and lipid metabolism disorders, but the mechanism is still under investigation. In this paper, we explored the effects of berberine on the weight, glucose levels, lipid metabolism, and serum insulin of KKAy mice and investigated its possible glucose and lipid-regulating mechanism. We randomly divided KKAy mice into two groups: berberine group (treated with 250 mg/kg/d berberine) and control group. Fasting blood glucose (FBG), weight, total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-c), low-density lipoprotein-cholesterol (LDL-c), and fasting serum insulin were measured in both groups. The oral glucose tolerance test (OGTT) was performed. RT(2) PCR array gene expression analysis was performed using skeletal muscle of KKAy mice. Our data demonstrated that berberine significantly decreased FBG, area under the curve (AUC), fasting serum insulin (FINS), homeostasis model assessment insulin resistance (HOMA-IR) index, TC, and TG, compared with those of control group. RT(2) profiler PCR array analysis showed that berberine upregulated the expression of glucose transporter 4 (GLUT4), mitogen-activated protein kinase 14 (MAPK14), MAPK8(c-jun N-terminal kinase, JNK), peroxisome proliferator-activated receptor α (PPARα), uncoupling protein 2 (UCP2), and hepatic nuclear factor 4α(HNF4α), whereas it downregulated the expression of PPARγ, CCAAT/enhancer-binding protein (CEBP), PPARγ coactivator 1α(PGC 1α), and resistin. These results suggest that berberine moderates glucose and lipid metabolism through a multipathway mechanism that includes AMP-activated protein kinase-(AMPK-) p38 MAPK-GLUT4, JNK pathway, and PPARα pathway.

[Effect of tianma gouteng recipe on interfering LV and aortic hypertrophy in renovascular hypertension rats].

OBJECTIVE: To investigate the effect of Tianma Gouteng recipe (TGR) on interfering left ventricular (LV) and aortic hypertrophy and tissue angiotensin II (Ang II) in rats with renovascular hypertension. METHOD: The animal model of renovascular hypertension was used in this experiment. Hypertensive rats were randomly allocated into model group, Enalapril group and TGR group, and the drugs were used for 6 weeks continuously. During this period, the blood pressure of rats was measured every two weeks. After rats were sacrificed, the wet weight, tissue Ang II level of LV and aorta, and the cardiac index were measured. RESULT: One week after renovascular stenosis, the systolic blood pressure (SPS) of model group was increased by 37.4 mmHg, and 7 weeks after stenosis, the LV and aortic hypertrophy was obvious increased, meanwhile, tissue Ang II of LV and aorta was raised markedly (P < 0.01). Contrasting with the model group, blood pressure was reduced and the morphological index was improved in Enalapril group respectively (P < 0.05 or P < 0.01); the wet weight of LV and aorta were reduced, the morphological index was improved, the rise of Ang II in tissue was suppressed, in TGR group significantly. CONCLUSION: TGR can attenuate myocardial and aorta hypertrophy induced by renovascular hypertension, and suppress the rise of Ang II in tissue significantly. This suggests that TGR has the effects on interfering LV and aortic hypertrophy by an independent-antihypertensive way.

[Effects of Tianzhi Keli on extracellular acetylcholine and catecholamine levels in striatum of rats with neuromitochondrial impairment].

OBJECTIVE: To investigate the effects of Tianzhi Keli (TZ) on acetylcholine (ACh) and catecholamine levels in striatum of rats with neuromitochondrial impairment, and try to find out the neuroprotective mechanism of TZ. METHOD: The microdialysis and high performance liquid chromatography (HPLC)-post column Immobilized enzyme reactor (IMER)-electrochemical detection (ED) were used to establish a model of mitochondrial energy metabolism impairment which induced by perfusion with sodium azide (NaN3), and measure continuously the effects of TZ on extracellular ACh, choline (Ch) and catecholamine of model rats. RESULT: After perfusion with NaN3, ACh, noradrenalin (NE), adrenaline (E), dopamine (DA), 3,4-Dihydroxyphenyl-aletic (DOPAC), and homovanillic acid (HVA) levels were decreased obviously (P < 0.05-0.01), while Ch level was increased distinctly (P < 0.01). Transmitters levels were recovered individually after stop the perfusion with NaN3. TZ can postpone the decrease of ACh and advance the recover of Ch. The effect of TZ coupled with duxil on increasing ACh level is more obviously than effect of TZ or duxil. TZ is also showing a tendency to postpone the decrease of catecholamine and advance its recovery. TZ coupled with duxil can advance the recovery of DOPAC and adjust the metabolic abnormity positively. CONCLUSION: TZ has effect on protecting impairment of choline neurosystem, which induced by damage of mitochondrion and abnormity of energy metabolism; coupled with duxil have synergistic action. TZ also has tendency to protect the impairment of epinephrine and dopamine neurosystem.

[Research progress of neuroprotective mechanisms of Gastrodia elata and its preparation].

The effects of Gastrodia elata on preventing decrepitude and advancing memory are closely associated with its neuroprotective activity. Previous researches proved that G. elata, its active components and preparations played a neuroprotective role by affecting the excitotoxicity, nitric monoxide (NO) system, neuroglia, biomembrane, oxidative neurotoxicity, apoptosis et al. Recent researches also suggest that reducing energy metabolism impairment, anti-inflammatory and immune modulating function may be new research targets of neuroprotective mechanism of G. elata.

[Effects of tianma gouteng fang on transmitter amino acids in the hippocampus extracellular liquids in freely moving rats subjected to brain ischemia].

OBJECTIVE: To observe the effects of Tianma Gouteng Fang (TGF) on the transmitter amino acids in the hippocampus extracellular liquids in freely moving rats subjected to incomplete brain ischemia. METHOD: Hippocampus extracellular liquids was collected continuously by the microdialysis sampling technology in freely moving rats during pre-ischemia, incomplete ischemia and reperfusion periods induced by the occlusion and loose of both common carotid arteries. Each dialysate sample was assayed for GABA, Tau, Glu, Cys and Arg with HPLC-electrochemical detector. RESULT: TGF increased the concentrations of GABA and Tau in the extracellular liquids of rat hippocampus. Compared with the model group, the concentration of Glu in the middle and large dosage groups of TGF, during the 120 min of ischemia, reduced by 38.64% and 31.35%, Tau increased by 13.99% and 12.86%, GABA advanced 25.89% and 33.99%, Cys decreased by 40.93% and 42.08%, Arg raised to 116.95% and 108.96%, respectively. After 120 min of reperfusion, the concentration of Glu decreased by 14.55% and 11.48%, Tau increased by 16.13% and 14.03%, GABA increased by 24.41% and 26.22%, respectively. CONCLUSION: TGF can increase the concentration of inhibitory amino acids in hippocampus extracellular liquids of rats and inhibit the excessive release of excitatory amino acids and raise the concentration of the inhibitory amino acids and Arg during the ischemia-reperfusion periods. Therefore, TGF can play the neuroprotective role.

[The effect of shourong compound formula on levels of dopamine and its metabolites in brain of Parkinson's disease mice induced by reserpine].

OBJECTIVE: To investigate the effect of Shourong compound formula on treating Parkinson's disease. METHOD: Parkinson's disease model mice induced by reserpine was used and by HPLC-ED the levels of Dopamine (DA) and its metabolites were determined. RESULT: Madopar could increase the levels of DA in brain of PD mice. The effect of madopar together with Sourong compound formula was better than that of madopar(P < 0.001). CONCLUSION: Shourong compound formula together with madopar has synergic effect on increase of DA level in brain and can reduce clinic dose of madopar so that side effect of madopar can be decreased.