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Peng M.,Southwest University | Peng M.,Basic Laboratory for medical center | Chen M.,Southwest University | Chen R.,Southwest University | And 3 more authors.
Journal of Medicinal Plants Research

Hydroxymethylbutenyl 4-diphosphate reductase (HDR) catalyzes the last reaction of the methylerythritol phosphate (MEP) pathway for the biosynthesis of artemisinin precursors, a branching step that separately produces isopentenyl diphosphate (IPP) and dimethylallyl diphosphate (DMAPP) in a ratio of 5:1 to 6:1. The full-length cDNA sequence of HDR was cloned and characterized from Artemisia annua L. for the first time. The new cDNA was designated as AaHDR (GenBank accession No.: GQ119345). The full-length cDNA of AaHDR was 1640 bp containing a 1368 bp open reading frame (ORF) encoding a polypeptide of 455 amino acids with a calculated molecular mass of 51.3 KDa and an isoelectric point of 5.63. Comparative and bioinformatic analysis revealed that AaHDR had extensive homology with HDRs from other plant species and contained a conserved transit peptide for plastids. The phylogenetic analysis indicated that all HDRs could be divided into three groups and AaHDR belonged to plant HDRs family. Then the homology-based structural modeling of AaHDR showed that AaHDR had the typical structure of HDR from A. aeolicus, which adopted a cloverleaf or trefoil-like structure with each monomer in the dimer containing three alpha/beta domains surrounding a central [Fe 3S 4] cluster ligated to Cys13, Cys96 and Cys193. Finally, AaHDR was transformed into the E. coli HDR mutant strain MG1655 ara< >HDR, which was able to rescue the lethal phenotype of the E. coli HDR mutant strain MG1655 ara-HDR. This confirmed that AaHDR had the typical function of HDR gene. The cloning and characterization of AaHDR will be helpful to understand more about the function of HDR at the level of molecular genetics and unveil the biosynthetic mechanism of artemisinin precursors. The present work also provides a candidate gene for metabolic engineering of the artemisinin biosynthesis pathway in A. annua. © 2011 Academic Journals. Source

Peng M.-F.,Basic Laboratory for medical center | Peng M.-F.,China Institute of Technology | Li K.,Basic Laboratory for medical center | Wang C.,Basic Laboratory for medical center | And 2 more authors.
BMC Complementary and Alternative Medicine

Background: Electroacupuncture (EA) is one of the techniques of acupuncture and is believed to be an effective alternative and complementary treatment in many disorders. The aims of this study were to investigate the effects and mechanisms of EA at acupoint Zusanli (ST36) on the plasticity of interstitial cells of Cajal (ICCs) in partial bowel obstruction.Methods: A Sprague Dawley rat model of partial bowel obstruction was established and EA was conducted at Zusanli (ST36) and Yinglingquan (SP9) in test and control groups, respectively. Experiments were performed to study the effects and mechanisms of EA at Zusanli on intestinal myoelectric activity, distribution and alteration of ICCs, expression of inflammatory mediators, and c-Kit expression.Results: 1) EA at Zusanli somewhat improved slow wave amplitude and frequency in the partial obstruction rats. 2) EA at Zusanli significantly stimulated the recovery of ICC networks and numbers. 3) the pro-inflammatory mediator TNF-α and NO activity were significantly reduced after EA at Zusanli, However, no significant changes were observed in the anti-inflammatory mediator IL-10 activity. 4) EA at Zusanli re-expressed c-Kit protein. However, EA at the control acupoint, SP9, significantly improved slow wave frequency and amplitude, but had no effect on ICC or inflammatory mediators.Conclusions: We concluded that EA at Zusanli might have a therapeutic effect on ICC plasticity, and that this effect might be mediated via a decrease in pro-inflammatory mediators and through the c-Kit signaling pathway, but that the relationship between EA at different acupoints and myoelectric activity needs further study. © 2014 Peng et al. Source

Jin F.,General Hospital of PLA Chengdu Military Area Command | Jin F.,Luzhou Medical College | Jiang S.,General Hospital of PLA Chengdu Military Area Command | Jiang S.,Luzhou Medical College | And 7 more authors.
Biochemical and Biophysical Research Communications

Saturated fatty acids (FA) have been linked to an increased risk of cardiovascular disease. The effects of acipimox, a FA-lowering agent, on palmitate- (an important saturated fatty acid) stimulated atherosclerosis remains to be elucidated. We investigated the effects of acipimox on atherosclerosis in ApoE-/- mice fed a palmitate-rich diet. Male ApoE-/- mice, 6-8weeks of age, were randomized into three groups. The animals were fed a normal chow diet in the control group, a diet containing 5% palmitic acid in the palmitate group, and a diet containing 5% palmitic acid and 0.02% acipimox in the acipimox group. The plasma lipid profiles, aortic lesions, plaque collagen content and the expression of matrix metalloproteinase (MMP)-2, MMP-3, MMP-9, and MMP-14 and the tissue inhibitor of MMP (TIMP)-1, and TIMP-2 were determined after a 12-week treatment. The palmitate-rich diet significantly increased plasma FA concentrations (P<0.01), enhanced atherosclerotic lesions (P<0.01), decreased plaque collagen content (P<0.01) and upregulated MMP-2 (P<0.05) in the aorta. Additionally, all of these harmful effects were significantly attenuated by co-treatment with acipimox (P<0.05 or P<0.01). The present study suggests that acipimox attenuates atherosclerosis and enhances plaque stability in ApoE-/- mice fed a palmitate-rich diet. © 2012 Elsevier Inc. Source

Jiang S.,General Hospital of PLA Chengdu Military Area Command | Jiang S.,Luzhou Medical College | Jin F.,General Hospital of PLA Chengdu Military Area Command | Jin F.,Luzhou Medical College | And 7 more authors.
High Altitude Medicine and Biology

Jiang, Sihua, Feipeng Jin, De Li, Xingmei Zhang, Yun Yang, Dachun Yang, Kun Li, Yongjian Yang, and Shuangtao Ma. Intermittent hypobaric hypoxia promotes atherosclerotic plaque instability in ApoE-deficient mice. High Alt Med Biol 14:175-180, 2013. - Aim: Sudden cardiac death is one of the most frequent causes of death at high altitude. It has been reported that the intermittent normobaric hypoxia experienced by patients with obstructive sleep apnea may enhance the development of atherosclerosis. However, the effect of hypobaric hypoxia, which mimics the ambient air at high altitude, in the development of atherosclerosis has not been investigated. Methods: Twenty male ApoE-deficient mice, 8 weeks of age, were subjected to either control conditions or intermittent hypobaric hypoxia (IHH) for 8 weeks. Mice in the IHH group were exposed to a hypobaric chamber that replicated the hypobaric hypoxia conditions found at 4000 m altitude for 8 hours a day. Results: IHH-exposed mice did not significantly differ from control mice in plasma lipid levels, including triglyceride, total cholesterol, low-density lipoprotein, and high-density lipoprotein. The hematoxylin and eosin-stained sections of the aortic root showed similar plaque size between the groups. However, IHH-treated mice exhibited significantly decreased plaque collagen content, a feature of atherosclerotic plaque stability. Additionally, matrix metalloproteinase (MMP)-9 protein expression was significantly increased, whereas tissue inhibitor of MMP (TIMP)-2 expression was decreased after exposure to IHH. Conclusion: IHH may promote atherosclerotic plaque instability in ApoE-deficient mice by changing the balance of MMPs and TIMPs. © Mary Ann Liebert, Inc. Source

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