Effect of resveratrol on gluconeogenesis in exercise-induced fatigue rats / 中国组织工程研究

BACKGROUND:Resveratrol is a natural antioxidant extracted from plants.Its mechanism of improving exercise-induced fatigue mainly focuses on the protective effect against oxidative stress and inflammation.In this study,the protective mechanism of resveratrol on exercise-induced fatigue was mainly discussed from the perspective of gluconeogenesis. OBJECTIVE:To investigate the effect of resveratrol on gluconeogenesis in exercise-induced fatigue rats. METHODS:After 1 week of adaptive training,male Sprague-Dawley rats were randomly divided into 4 groups with 12 rats in each group:blank control group,resveratrol group,exercise group,resveratrol + exercise group.Weight-bearing swimming training was used to simulate long-term medium-high intensity exercise.After swimming with a weight of 5%for 1 hour every day,50 mg/kg resveratrol solution or the same volume of dimethyl sulfoxide solvent were given orally,6 days a week,for a total of 6 weeks.Samples were collected 24 hours after the last exercise,and the levels of urea nitrogen,creatine kinase,blood glucose,liver glycogen and lactic acid and pyruvate in liver tissue were detected by the kit.The activity of phosphoenolpyruvate carboxykinase was detected by microassay,and the activity of glucose-6-phosphatase was detected by enzyme-linked immunosorbent assay.Real-time fluorescence quantitative PCR was used to detect the gene expression of silent information regulator 1,cAMP-response element binding protein and peroxisome proliferator-activated receptor-γ coactivator-1α. RESULTS AND CONCLUSION:In the exercise group,plasma urea nitrogen and creatine kinase levels of rats were significantly increased(both P<0.05),liver lactate and pyruvate levels and lactate/pyruvate ratio were significantly increased(all P<0.01),and blood glucose and liver glycogen contents were significantly decreased(both P<0.01).Resveratrol supplementation could effectively improve the above conditions.Exercise significantly decreased the activities of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase(P<0.01,P<0.05),and resveratrol supplementation significantly increased the activity of phosphoenolpyruvate carboxykinase in liver tissue(P<0.01).The mRNA expression levels of silent information regulator 1,cAMP-response element binding protein and peroxisome proliferator-activated receptor-γ coactivator-1α in liver tissue of the exercise group were significantly decreased(all P<0.01),while resveratrol supplementation could significantly increase the gene expression levels of this pathway.To conclude,resveratrol can relieve exercise-induced fatigue caused by long-term medium-high intensity exercise,and its mechanism may be related to up-regulating the gluconeogenesis regulatory pathway,improving rate-limiting enzyme activity,promoting liver gluconeogenesis,and increasing blood glucose and liver glycogen levels.

Discovery of a highly efficient TylF methyltransferase via random mutagenesis for improving tylosin production.

Macrolides are currently a class of extensively used antibiotics in human and animal medicine. Tylosin is not only one of the most important veterinary macrolides but also an indispensable material for the bio- and chemo-synthesis of new generations of macrolide antibiotics. Thus, improving its production yield is of great value. As the key rate-limiting enzyme catalyzing the terminal step of tylosin biosynthesis in Streptomyces fradiae (S. fradiae), TylF methyltransferase's catalytic activity directly affects tylosin yield. In this study, a tylF mutant library of S. fradiae SF-3 was constructed based on error-prone PCR technology. After two steps of screening in 24-well plates and conical flask fermentation and enzyme activity assay, a mutant strain was identified with higher TylF activity and tylosin yield. The mutation of tyrosine to phenylalanine is localized at the 139th amino acid residue on TylF (TylFY139F), and protein structure simulations demonstrated that this mutation changed the protein structure of TylF. Compared with wild-type protein TylF, TylFY139F exhibited higher enzymatic activity and thermostability. More importantly, the Y139 residue in TylF is a previously unidentified position required for TylF activity and tylosin production in S. fradiae, indicating the further potential to engineer the enzyme. These findings provide helpful information for the directed molecular evolution of this important enzyme and the genetic modification of tylosin-producing bacteria.

Atorvastatin attenuates allergic inflammation by blocking prostaglandin biosynthesis in rats with allergic rhinitis.

BACKGROUND: Prostaglandins (PGs) are bioactive lipid mediators derived from the nuclear and plasma membranes via the cyclooxygenase (COX) pathway of arachidonic acid (AA) metabolism. PGs bridge the interactions between various immunomodulatory cells in allergic rhinitis (AR) and are considered key players in regulating pro-inflammatory and anti-inflammatory responses. AA conversion to PGs involves rate-limiting enzymes that may be blocked by statins. The mechanisms by which statins regulate these enzymes in AR remain unclear. We investigated the effects of oral atorvastatin on PGs production in AR. METHODS: An ovalbumin-induced AR rat model was constructed and the changes in nasal symptom score and nasal mucosa histopathological characteristics of AR rats under different atorvastatin doses were assessed. qRT-PCR, western blotting, and immunofluorescence were used to detect the mRNA and protein expression levels of rate-limiting enzymes and downstream molecules of AA metabolism in the nasal mucosa and liver. RESULTS: Oral atorvastatin significantly alleviated symptoms and eosinophil infiltration in the nasal mucosa, inhibited goblet cell hyperplasia and mast cell recruitment, and decreased mucus secretion in AR rats. Increasing atorvastatin dose increased the anti-inflammatory effects. High-dose atorvastatin inhibited upregulation of the inflammatory mediator PGD2 in the nasal mucosa of AR rats. Compared to the control group, the mRNA and protein expression of the rate-limiting enzymes COX-2, PGDS, and PGES in AA metabolism in the AR group were upregulated but downregulated after the oral administration of high-dose atorvastatin. Atorvastatin also showed dose-dependent inhibition of ERK1/2 and downstream NF-κB phosphorylation in the nasal mucosa and liver of AR rats. CONCLUSIONS: Atorvastatin inhibited allergic inflammation and attenuated AR nasal symptoms by downregulating PGD2 and rate-limiting enzyme expression in PGD2 biosynthesis, possibly by blocking the RAS/ERK/NF-κB signaling pathway.

Plasma and Urine Indoleamine 2,3-Dioxygenase Activity: Promising Biomarkers for Chronic Kidney Disease and Inflammation Status.

Purpose: Our aim was to determine the relationship between plasma and urine indoleamine 2.3-dioxygenase (IDO) activity and stage of chronic kidney disease (CKD). Patients and Methods: Demographic and clinical parameters, including plasma and urine IDO activity, were recorded in 47 CKD patients and 30 controls. One-way ANOVA with the least significant difference method was used to compare means of variables that had normal distributions and homogeneous variance. Variables with non-normal distributions were log-transformed and compared using the rank sum test Pearson or Spearman correlation coefficients were determined. Binary logistic regression and ordinal logistic regression were used to identify independently significant factors. Receiver operating characteristic (ROC) analysis was performed. Results: The control group had higher levels of hemoglobin and albumin and lower levels of creatinine and blood urea nitrogen (BUN; all P<0.01). The level of highly sensitive C reactive protein (hs-CRP) increased as CKD stage increased (P<0.01). Plasma and urine IDO activity were positively correlated (r=0.7, P<0.01). Plasma IDO activity correlated with age, creatinine, BUN, triglycerides, uric acid, albumin, and hemoglobin (all P<0.05); urine IDO activity correlated with age, BMI, creatinine, BUN, and hemoglobin (all P< 0.05). There were positive correlations of hs-CRP level with plasma IDO activity and urine IDO activity (both P<0.01). After adjusting for CKD-related factors, plasma IDO activity, urine IDO activity, and hs-CRP were independent risk factors for CKD (all P<0.05). Ordinal logistic regression also indicated that plasma and urine IDO activity were significantly associated with CKD stage. ROC analysis indicated that plasma and urine IDO activity were good predictors of CKD and distinguished different stages of CKD. There was a strong correlation between plasma IDO activity and inflammatory status in patients with CKD (OR=1258.908, P<0.01). Conclusion: Plasma and urine IDO activity have potential use as biomarkers for early-stage CKD, progression of CKD, and inflammation status.

A Resource to Infer Molecular Paths Linking Cancer Mutations to Perturbation of Cell Metabolism.

Some inherited or somatically-acquired gene variants are observed significantly more frequently in the genome of cancer cells. Although many of these cannot be confidently classified as driver mutations, they may contribute to shaping a cell environment that favours cancer onset and development. Understanding how these gene variants causally affect cancer phenotypes may help developing strategies for reverting the disease phenotype. Here we focus on variants of genes whose products have the potential to modulate metabolism to support uncontrolled cell growth. Over recent months our team of expert curators has undertaken an effort to annotate in the database SIGNOR 1) metabolic pathways that are deregulated in cancer and 2) interactions connecting oncogenes and tumour suppressors to metabolic enzymes. In addition, we refined a recently developed graph analysis tool that permits users to infer causal paths leading from any human gene to modulation of metabolic pathways. The tool grounds on a human signed and directed network that connects ∼8400 biological entities such as proteins and protein complexes via causal relationships. The network, which is based on more than 30,000 published causal links, can be downloaded from the SIGNOR website. In addition, as SIGNOR stores information on drugs or other chemicals targeting the activity of many of the genes in the network, the identification of likely functional paths offers a rational framework for exploring new therapeutic strategies that revert the disease phenotype.

N-3 Polyunsaturated Fatty Acid Dehydrogenase Fat-1 Regulates Mitochondrial Energy Metabolism by Altering DNA Methylation in Isolated Cells of Transgenic Cattle.

The fatty acid dehydrogenase fat-1 gene, derived from Caenorhabditis elegans, encodes n-3 polyunsaturated fatty acid dehydrogenase (Δ15 desaturase) and catalyzes the 18-20-carbon n-6 polyunsaturated fatty acids (n-6 PUFA) to generate corresponding n-3 polyunsaturated fatty acids (n-3 PUFA). Subsequently, fat-1 can influence the n-6: n-3 PUFA ratio in fat-1 transgenic cells. This study aimed to explore which processes of energy metabolism are affected exogenous fat-1 transgene and the relationship between these effects and DNA methylation. Compared with the wild-type group, the n-3 PUFA content in fat-1 transgenic bovine fetal fibroblasts was significantly increased, and the n-6 PUFA content and the n-6: n-3 PUFA ratio decreased. In the context of energy metabolism, the increase of exogenous fat-1 transgene decreased ATP synthesis by 39% and reduced the activity and expression of key rate-limiting enzymes in glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation, thus weakening the cells' capacity for ATP production. DNA methylation sequencing indicated that this inhibition of gene expression may be due to altered DNA methylation that regulates cell energy metabolism. Exogenous fat-1 transgenic cells showed changes in the degree of methylation in the promoter region of genes related to energy metabolism rate-limiting enzymes. We suggest that alters the balance of n-6/n-3 PUFA could regulate altered DNA methylation that affect mitochondrial energy metabolism.

NaAsO2 decreases GSH synthesis by inhibiting GCLC and induces apoptosis through Hela cell mitochondrial damage, mediating the activation of the NF-κB/miR-21 signaling pathway.

BACKGROUND: Cervical cancer is the fourth most common cancer in women worldwide, and arsenic has a certain effect in solid tumor chemotherapy. As the rate-limiting enzyme subunit of GSH synthesis, GCLC may be an important target for arsenic to induce apoptosis through mitochondrial apoptosis pathway to exert anti-tumor effect. NF-κB plays an important role in the occurrence and development of cervical cancer and can regulate the expression of GCLC. miR-21 is a potential biomarker of cervical cancer, which can induce apoptosis through ROS regulated the mitochondrial pathway of cells. However, the role of miR-21 in the mitochondrial pathway of cervical cancer cells induced by NaAsO2 through NF-κB/GCLC and GSH synthesis regulated oxidative stress is rarely reported. Therefore, the purpose of this study was to investigate whether NaAsO2 might induce mitochondrial damage and apoptosis of cervical cancer cells through NF-κB/ miR-21 /GCLC induced oxidative stress, and play the anti-tumor role of arsenic as a potential drug for the treatment of cervical cancer. METHODS: Hela cells were treated with different concentrations of NaAsO2, D, L-Buthionine-(SR)-sulfoximine (BSO), IκBα inhibitor (BAY 11-7082) and miR-21 Inhibitor. CCK-8 assay, Western Blot, qRT PCR, immunofluorescence, transmission electron microscopy, mitochondrial Membrane Potential Assay Kit with JC-1,2',7'-Dichlorofluorescin diacetate fluorescent probe and Annexin V-FITC were used to measure cell activity, GSH and ROS, mitochondrial morphology and membrane potential (ΔΨm), protein and mRNA expression of GCLC, GCLM, p65, IκBα, p-P65, p-I κBα, Bcl-2, BAX, Caspase3, cleaved-caspase3 and miR-21. RESULTS: Compared with the control group, with the gradual increasing dose of NaAsO2, cell viability was considerable reduced, and increased rate of apoptosis, intracellular GSH level was decreased significantly, ROS was increased, mitochondrial structure was damaged, mitochondrial membrane potential ΔΨm and Bcl2/BAX lowered, the expression of Caspase3 and cleaved-caspase3 were significantly increased, resulting in mitochondrial apoptosis. When Hela cells were treated with 15, 20, and 25 µmol/L NaAsO2, the mRNA and protein levels of GCLC and GCLM were reduced, the expression of p65 in the nucleus was increased, the expression of p-p65/p65, p-IκBα/IκBα and miR-21 were significantly increased. When BSO increased the inhibitory effect of NaAsO2 on GCLC, Compared with NaAsO2 group, the ΔΨm and protein of Bcl-2/BAX, caspase3 and cleaved-capsase3 were increased. When BAY 11-7082 combined with NaAsO2 co-treated, compared with the NaAsO2 group, the protein and mRNA expression of GCLC was increased, NaAsO2-increased expression level of miR-21 was suppressed, and the ΔΨm and cell viability were higher. In addition, compared with the combination of NaAsO2 and miR-21NC, the protein expression of GCLC was increased, the ΔΨm and cell viability reduction were alleviated by miR-21 Inhibitor combined with NaAsO2. CONCLUSION: NaAsO2 may lead to ROS accumulation in Hela cells and trigger mitochondrial apoptosis. The mechanism may be related to the activation of NF-κB signaling pathway and the promotion of miR-21 expression which leads to the inhibition of GCLC expression and the significant decrease of intracellular reductive GSH synthesis.

The new chimeric chiron genes evolved essential roles in zebrafish embryonic development by regulating NAD+ levels.

The origination of new genes is important for generating genetic novelties for adaptive evolution and biological diversity. However, their potential roles in embryonic development, evolutionary processes into ancient networks, and contributions to adaptive evolution remain poorly investigated. Here, we identified a novel chimeric gene family, the chiron family, and explored its genetic basis and functional evolution underlying the adaptive evolution of Danioninae fishes. The ancestral chiron gene originated through retroposition of nampt in Danioninae 48-54 million years ago (Mya) and expanded into five duplicates (chiron1-5) in zebrafish 1-4 Mya. The chiron genes (chirons) likely originated in embryonic development and gradually extended their expression in the testis. Functional experiments showed that chirons were essential for zebrafish embryo development. By integrating into the NAD+ synthesis pathway, chirons could directly catalyze the NAD+ rate-limiting reaction and probably impact two energy metabolism genes (nmnat1 and naprt) to be under positive selection in Danioninae fishes. Together, these results mainly demonstrated that the origin of new chimeric chiron genes may be involved in adaptive evolution by integrating and impacting the NAD+ biosynthetic pathway. This coevolution may contribute to the physiological adaptation of Danioninae fishes to widespread and varied biomes in Southeast Asian.

Regulation of Hypnotic Active Components of Cnidii Fructus on Melatonin Synthesis Rate-limiting Enzyme AANAT in Rats with PCPA-induced Insomnia / 中国实验方剂学杂志

Objective:To observe the effects of Cnidii Fructus hypnotic active components （CHC） on the behaviors of rats with p-chlorophenylalanine （PCPA）-induced insomnia and melatonin （MT） synthesis rate-limiting enzyme arylalkylamine <italic>N</italic>-acetyltransferase （AANAT）， and explore the protective mechanism of CHC on the pineal gland. Method:Male SD rats of SPF grade were randomly divided into a blank control group， a model group， a MT group， and high-， medium-， and low-dose CHC groups with 10 rats in each group. Except for the blank control group， other groups received 4.5% PCPA suspension at 10 mL·kg^-1， intragastric administration， for two consecutive days. After PCPA model of insomnia was established， normal and model groups were gavaged at the same volume of 2% Tween-80， MT control group （10 mg·kg^-1）， CHC was high， medium and low （60， 30， 15 mg·kg^-1）， 10 mL·kg^-1， once a day， for consecutive 7 days. Four days after administration， open field， elevated cross maze， and pentobarbital sodium-induced sleep tests were conducted， respectively. Serum MT was detected by enzyme-linked immunosorbent assay. The mRNA expression level of AANAT was determined by real-time fluorescence-based quantitative polymerase chain reaction （Real-time PCR）. The expression of AANAT protein in the pineal gland was detected by Western blot. Result:Compared with the results in the blank control group， the total distance of open field activity and standing times and duration in the central area were increased （<italic>P</italic><0.05， <italic>P</italic><0.01）， the proportions of open arm entry （OE%） and open arm time （OT%） were decreased （<italic>P</italic><0.05）， and the sleep latency was prolonged （<italic>P</italic><0.01） in the model group. Compared with the model group， no significant difference was observed in the low-dose CHC group， while other groups exhibited reduced total distance of activity （<italic>P</italic><0.05， <italic>P</italic><0.01）， elevated OE% （<italic>P</italic><0.05）， shortened sleep latency， and prolonged sleep time （<italic>P</italic><0.05， <italic>P</italic><0.01）. Compared with the serum MT in the blank control group， that in the model group was decreased （<italic>P</italic><0.01）. Compared with the model group， no significant difference was observed in the low-dose CHC group， while other groups displayed increased serum MT （<italic>P</italic><0.05）. The mRNA and protein expression of AANAT was decreased in the model group as compared with that in the blank control group （<italic>P</italic><0.01）. Compared with the model group， the MT group and the high-dose CHC group showed up-regulated expression （<italic>P</italic><0.05）. Conclusion:CHC improved the behavioral indexes of PCPA-induced insomnia， increased the synthesis and secretion of MT in pineal cells， and elevated the serum MT level， which was related to the up-regulation of the mRNA and protein expression of AANAT in the pineal gland.

The Biokinetic Spectrum for Temperature and optimal Darwinian fitness.

Darwinian fitness is maximised at a temperature below Topt, but what this temperature is remains unclear. By linking our previous work on the Biokinetic Spectrum for Temperature with a model for temperature-dependent biological growth rate we obtain a plausible value for such a temperature. We find this approach reveals considerable commonalities in how life responds to temperature with implications that follow in evolution, physiology and ecology. We described a data set consisting of 17,021 observations of temperature-dependent population growth rates from 2411 bacterial, archaeal and eukaryal strains. We fitted a thermodynamic model to describe the strains' temperature-dependent growth rate curves that assumed growth was limited by a single rate-limiting enzyme. We defined Umes as an empirical measure of the temperature at which strains grew as fast and also as efficiently as possible. We propose that Darwinian fitness is optimised at Umes by trading-off growth rate and physiological efficiency. Using the full data set we calculated the Biokinetic Spectrum for Temperature (BKST): the distribution of temperature-dependent growth rates for each temperature. We used quantile regression to fit alternative models to the BKST to obtain quantile curves. A quantile is a value that contains a particular proportion of the data. The quantile curves suggested commonalities in temperature-dependencies spanning taxa and ecotype, consistent with the single rate-limiting enzyme concept. We showed that on the log scale, the slopes of the quantile curves were the same as the slopes of the thermodynamic model growth curves at Umes. This was true for Bacteria, Archaea, and Eukarya, and across other conditions (pH, water activity, metabolic type and trophic type). We showed that the quantile curves were the loci of the temperatures and growth rates that optimised Darwinian fitness for each strain at a given temperature-dependence and independently of other conditions. The quantile curves for Archaea and Bacteria shared a number of similarities attributable to the influence of the properties of water on protein folding. Other implications have impact on evolutionary biology, ecology, and physiology. The model predicts the existence of eurythermic strains that grow with about equal efficiency over a broad temperature range. These strains will have higher evolutionary rates with lower mutational costs that are independent of environmental conditions, a factor likely to have been significant during the Precambrian if the early Earth was warmer than today. The model predicts that random mutations are likely to result in shifts along the quantile curves and not across them. It predicts that some psychrophiles will be capable of performing well under climate change, and that selection will favour faster growth rates as the temperature increases. Last, it predicts trade-offs between growth rate and soma production, so that temperature-dependence, and possibly Darwinian fitness, remain constant over a broad temperature range and growth rates.

Effects of chilling stress on the accumulation of soluble sugars and their key enzymes in Jatropha curcas seedlings.

As osmolytes and signaling molecules, soluble sugars participate in the response and adaptation of plants to environmental stresses. In the present study, we measured the effect of chilling (12 °C) stress on the contents of eight soluble sugars in the leaves, cotyledons, stems, and roots of Jatropha curcas seedlings, as well as on the activities of eight rate-limiting enzymes that are critical to the metabolism of those soluble sugars. Chilling stress promoted both starch hydrolysis and soluble sugar accumulation. The soluble sugar contents of the leaves and cotyledons were affected more than that of the stems and roots. Meanwhile, the activities of the corresponding metabolic enzymes (e.g., ß-amylase, uridine diphosphate glucose phosphorylase, and sucrose phosphate synthase) also increased in some organs. The gradual increase of soluble neutral alkaline invertase activity in the four studied organs suggested that sucrose catabolic production, such as glucose and fructose, was especially important in determining resistance to chilling stress and hexose signal transduction pathway. In addition, the substantial accumulation of raffinose family oligosaccharides and increase in corresponding metabolic enzyme activity suggested that galactinol and raffinose play an important role in determining the chilling resistance of J. curcas. Together, these findings establish a foundation for determining the relationship between the chilling resistance and soluble sugar accumulation of J. curcas and for investigating the mechanisms underlying sugar signaling transduction and stress responses.

Correlative analysis of plasma SN-38 levels and DPD activity with outcomes of FOLFIRI regimen for metastatic colorectal cancer with UGT1A1 *28 and *6 wild type and its implication for individualized chemotherapy.

It remains uncertain whether there is an correlation between clinical pharmacokinetic parameters and outcomes for metastatic colorectal cancer especially with UGT1A1 *28 and *6 wild type (*1/*1-*1/*1) for serious events associated with Irinotecan are largely excluded. This study retrospectively analyzed the relationship between Irinotecan metabolite levels and outcomes of UGT1A1 *1/*1-*1/*1 genotype arrangement. Blood samples (n = 244) were collected for analysis of plasma DPD activity (before first chemotherapy) and SN-38 levels (1.5 and 49 hour after CPT-11 administration). Clinical variables such as toxicity and outcomes were then assessed. Of the *1/*1 -*1/*1 genotype combination, the median progression free survival of the CSN-38 1.5 h > 50.24 ng/ml subset was remarkably longer than that of the CSN-38 1.5 h ≤ 50.24 ng/ml subset. However, there were no differences between the CSN-38 49 h > 15.25 ng/ml subgroup and the ≤ 15.25 ng/ml group. It was lower DPD activity that responsible for the relatively higher incidence of bone marrow hypocellular, diarrhea, and oral mucositis in the CSN-38 1.5 h > 50.24 ng/ml and CSN-38 49 h > 15.25 ng/ml subsets. Therefore, plasma SN-38 levels is related to outcomes for UGT1A1 *1/*1-*1/*1 genotype, to improve efficacy, patients with CSN-38 1.5 h lower than 50.24 ng/ml, CPT-11 dosage could be added in next chemmotherapy on SN-38 plasma level monitoring. Additionally, in patients with DPD activity below 3.18 before treatment, appropriate reduction of 5-FU dose could be considered to minimize the incidence of adverse events.

[Analysis of metabolic pathway of terpenoids in Blumea balsamifera].

In order to provide a theoretical basis for the regulation of active ingredient, the terpenoids metabolic pathway and specific enzymes in Blumea balsamifera are investigated. Basing on transcriptome information, B. balsamifera terpenoids metabolic pathway was analyzed in KEGG data base. Four metabolic pathway of terpenoids were found in KEGG data base. They were terpenoid backbone biosynthesis, monoterpenoid biosynthesis, diterpenoid biosynthesis, sesquiterpenoid and triterpenoid biosynthesis, contained 103, 10, 29,59 genes, respectively. Through the analysis of the enzyme and product in the pathway, the result showed that there were 8 kinds of monoterpenes, 3 kinds of diterpenes, 3 kinds of triterpenes and sesquiterpenes. The mainly key enzymes were deoxyxylulose 5-phosphate synthase, HMG-CoA reductase and allyl transferase system. In B. balsamifera, there were relatively few monoterpenes synthetic enzymes, while the type of products was much more than other terpenes. This may be relate to the non-specific catalytic characteristic of monoterpene synthase. It is expected to improve the yield of terpenoids in B. balsamifera by analysis the pathways and regulation the key enzymes.

Analysis of metabolic pathway of terpenoids in Blumea balsamifera / 中国中药杂志

In order to provide a theoretical basis for the regulation of active ingredient, the terpenoids metabolic pathway and specific enzymes in Blumea balsamifera are investigated. Basing on transcriptome information, B. balsamifera terpenoids metabolic pathway was analyzed in KEGG data base. Four metabolic pathway of terpenoids were found in KEGG data base. They were terpenoid backbone biosynthesis, monoterpenoid biosynthesis, diterpenoid biosynthesis, sesquiterpenoid and triterpenoid biosynthesis, contained 103, 10, 29,59 genes, respectively. Through the analysis of the enzyme and product in the pathway, the result showed that there were 8 kinds of monoterpenes, 3 kinds of diterpenes, 3 kinds of triterpenes and sesquiterpenes. The mainly key enzymes were deoxyxylulose 5-phosphate synthase, HMG-CoA reductase and allyl transferase system. In B. balsamifera, there were relatively few monoterpenes synthetic enzymes, while the type of products was much more than other terpenes. This may be relate to the non-specific catalytic characteristic of monoterpene synthase. It is expected to improve the yield of terpenoids in B. balsamifera by analysis the pathways and regulation the key enzymes.