Kuan-Hung Lin

Chemical composition of seed oils in native Taiwanese Camellia species.

The aim of this study was to examine the fatty acid (FA) composition and levels in seeds of twelve native Camellia species collected in different populations of major producing regions in Taiwan. The constituents of FAs varied within and among populations. Oleic acid (OA) was found to be the predominant FA constituent in all species. Remarkably high levels of unsaturated OA and linoleic acid (LA), found in two populations of Camellia tenuiflora (CT), C. transarisanensis (CTA), and C. furfuracea (CFA), were similar to those reported for olive oil. The levels of saturated palmitic acid (PA) from most of the tested seed oils were less than 13%. Among the different fats, some FAs can be used as functional ingredients for topical applications. The seed oils of CT, CTA, and CFA possess chemical compounds that make them useful in health-oriented cooking due to their high OA and LA contents and low PA content.

Antioxidant activity of herbaceous plant extracts protect against hydrogenperoxide-induced DNA damage in human lymphocytes

BackgroundHerbaceous plants containing antioxidants can protect against DNA damage. Thepurpose of this study was to evaluate the antioxidant substances,antioxidant activity, and protection of DNA from oxidative damage in humanlymphocytes induced by hydrogen peroxide (H2O2). Ourmethods used acidic methanol and water extractions from six herbaceousplants, including Bidens alba (BA), Lycium chinense (LC),Mentha arvensis (MA), Plantago asiatica (PA),Houttuynia cordata (HC), and Centella asiatica(CA).MethodsAntioxidant compounds such as flavonol and polyphenol were analyzed.Antioxidant activity was determined by the inhibition percentage ofconjugated diene formation in a linoleic acid emulsion system and bytrolox-equivalent antioxidant capacity (TEAC) assay. Their antioxidativecapacities for protecting human lymphocyte DNA fromH2O2-induced strand breaks was evaluated by cometassay.ResultsThe studied plants were found to be rich in flavonols, especially myricetinin BA, morin in MA, quercetin in HC, and kaemperol in CA. In addition,polyphenol abounded in BA and CA. The best conjugated diene formationinhibition percentage was found in the acidic methanolic extract of PA.Regarding TEAC, the best antioxidant activity was generated from the acidicmethanolic extract of HC. Water and acidic methanolic extracts of MA and HCboth had better inhibition percentages of tail DNA% and tail moment ascompared to the rest of the tested extracts, and significantly suppressedoxidative damage to lymphocyte DNA.ConclusionQuercetin and morin are important for preventing peroxidation and oxidativedamage to DNA, and the leaves of MA and HC extracts may have excellentpotential as functional ingredients representing potential sources ofnatural antioxidants.

Tissue- and genotype-specific ascorbate peroxidase expression in sweet potato in response to salt stress.

The aim of this work was to study the short-term effects of salt stress on the antioxidant system and ascorbate peroxidase (APX) expression in two salt sensitive sweet potato cultivars Tainung 57 (TN57) and Tainung 66 (TN66), and one salt-tolerant cultivar Hsusu 18 (HS18). Plants were grown in plastic pots in a greenhouse for 30 d followed by NaCl treatments (0, 150, 300, and 450 mM) for 0, 24 and 48 h in a growth chamber. Young, fully expanded leaves of each treatment and period of time were clipped for enzyme activity measurements. In addition, different tissues (leaves, stems, and roots) were also harvested to analyze the tissue-specific APX gene expression using semiquantitative reverse-transcription polymerase chain reaction (RT-PCR). Three degenerated primers of APX isoforms from cytosol, peroxisomes and chloroplasts were used to amplify the APX complementary DNA of these cultivars. Our results show higher increase in APX activity at 24 and 48 h of salinity (450 mM of NaCl) in salt-stress tolerant genotype than in saltsensitive ones. The expression of APX isoforms in response to salinity was tissue specific and also dependent on stress duration.

PPARγ regulates the mitochondrial dysfunction in human neural stem cells with tumor necrosis factor alpha

Peroxisome proliferator-activated receptor gamma (PPARγ) belongs to a family of ligand-activated transcription factors, and its ligands are known to control many physiological and pathological conditions. The hypothesis of our study was that the PPARγ agonist (rosiglitazone) could mediate tumor necrosis factor alpha (TNFα) related to the regulation of human neural stem cells (hNSCs), by which TNFα possibly fulfills important roles in neuronal impairment. The results show that PPARγ mediates the cell viability of hNSCs via the downregulation of the activity of caspase 3, indicating that this rescue effect of PPARγ could improve the reduced levels of two mitochondrial regulators, adenosine monophosphate-activated protein kinase (AMPK) and Sirtuin 1 (SIRT1) in the hNSCs with TNFα. The stimulation of mitochondrial function by PPARγ was associated with activation of the PPAR coactivator1 alpha (PGC1α) pathway by up-regulation of oxidative defense and mitochondrial systems. The above protective effects appeared to be exerted by a direct activation of the rosiglitazone, because it protected hNSCs from TNFα-evoked oxidative stress and mitochondrial deficiency. Here we show that the rosiglitazone protects hNSCs against Aβ-induced apoptosis and promotes cell survival. These findings extend our understanding of the central role of PPARγ in TNFα-related neuronal impairment, which probably increases risks of neurodegenerative diseases. The anti-inflammatory effects of PPARγ in the hNSCs with TNFα, and the involved mechanisms were also characterized.

Chilling stress and chilling tolerance of sweet potato as sensed by chlorophyll fluorescence

We studied changes in the chlorophyll (Chl) fluorescence components in chilling-stressed sweet potato (Ipomoea batatas L. Lam) cv. Tainung 57 (TN57, chilling-tolerant) and cv. Tainung 66 (TN66, chilling-susceptible). Plants under 12-h photoperiod and 400 µmol m−2 s−1 irradiance at 24/20 °C (day/night) were treated by a 5-d chilling period at 7/7 °C. Compared to TN66, TN57 exhibited a significantly greater basic Chl fluorescence (F0), maximum fluorescence (Fm), maximum fluorescence yield during actinic irradiation (Fm′ ), and the quantum efficiency of electron transport through photosystem 2, PS2 (ΦPS2). Chilling stress resulted in decrease in the potential efficiency of PS2 (Fv/Fm), ΦPS2, non-photochemical fluorescence quenching (NPQ), non-photochemical quenching (qN), and the occurrence of chilling injury in TN66. Chilling increased the likelihood of photoinhibition, characterized by a decline in the Chl fluorescence of both cultivars, and photoinhibition during low temperature stress generally occurred more rapidly in TN66.

Rosiglitazone activation of PPARγ-dependent pathways is neuroprotective in human neural stem cells against amyloid-beta-induced mitochondrial dysfunction and oxidative stress.

Neuronal cell impairment, such as that induced by amyloid-beta (Aβ) protein, is a process with limited therapeutic interventions and often leads to long-term neurodegeneration common in disorders such as Alzheimers disease. Interestingly, peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-activated nuclear receptor whose ligands control many physiological and pathologic processes, and may be neuroprotective. We hypothesized that rosiglitazone, a PPARγ agonist, would prevent Aβ-mediated effects in human neural stem cells (hNSCs). Here, we show that rosiglitazone reverses, via PPARγ-dependent downregulation of caspase 3 and 9 activity, the Aβ-mediated decreases in hNSC cell viability. In addition, Aβ decreases hNSC messenger RNA (mRNA) levels of 2 neuroprotective factors (Bcl-2 and CREB), but co-treatment with rosiglitazone significantly rescues these effects. Rosiglitazone co-treated hNSCs also showed significantly increased mitochondrial function (reflected by levels of adenosine triphosphate and Mit mass), and PPARγ-dependent mRNA upregulation of PGC1α and mitochondrial genes (nuclear respiratory factor-1 and Tfam). Furthermore, hNSCs co-treated with rosiglitazone were significantly rescued from Aβ-induced oxidative stress and correlates with reversal of the Aβ-induced mRNA decrease in oxidative defense genes (superoxide dismutase 1, superoxide dismutase 2, and glutathione peroxidase 1). Taken together, these novel findings show that rosiglitazone-induced activation of PPARγ-dependent signaling rescues Aβ-mediated toxicity in hNSCs and provide evidence supporting a neuroprotective role for PPARγ activating drugs in Aβ-related diseases such as Alzheimers disease.

Beta-adrenoceptor pathway enhances mitochondrial function in human neural stem cells via rotary cell culture system

The structure and function of the human nervous system are altered in space when compared with their state on earth. To investigate directly the influence of simulated microgravity conditions which may be beneficial for cultivation and proliferation of human neural stem cells (hNSCs), the rotary cell culture system (RCCS) developed at the National Aeronautics and Space Administration (NASA) was used. RCCS allows the creation of a unique microgravity environment of low shear force, high-mass transfer and enables three-dimensional (3D) cell culture of dissimilar cell types. The results show that simulated microgravity using an RCCS would induce β-adrenoceptor, upregulate cAMP formation and activate both PKA and CREB (cAMP response element binding protein) pathways. The expression of intracellular mitochondrial genes, including PGC1α (PPAR coactivator 1α), nuclear respiratory factors 1 and 2 (NRF1 and NRF2) and mitochondrial transcription factor A (Tfam), regulated by CREB, were all significantly increased at 72 h after the onset of microgravity. Accordingly and importantly, the ATP level and amount of mitochondrial mass were also increased. These results suggest that exposure to simulated microgravity using an RCCS would induce cellular proliferation in hNSCs via an increased mitochondrial function. In addition, the RCCS bioreactor would support hNSCs growth, which may have the potential for cell replacement therapy in neurological disorders.

Rosiglitazone activation of PPARγ-dependent signaling is neuroprotective in mutant huntingtin expressing cells

Peroxisome proliferator-activated receptor gamma (PPARγ) is a crucial transcription factor for neuroprotection in several brain diseases. Using a mouse model of Huntingtons Disease (HD), we recently showed that PPARγ not only played a major function in preventing HD, but also oral intake of a PPARγ agonist (thiazolidinedione, TZD) significantly reduced the formation of mutant Huntingtin (mHtt) aggregates in the brain (e.g., cortex and striatum). The molecular mechanisms by which PPARγ exerts its HD neuroprotective effects remain unresolved. We investigated whether the PPARγ agonist (rosiglitazone) mediates neuroprotection in the mHtt expressing neuroblastoma cell line (N2A). Here we show that rosiglitazone upregulated the endogenous expression of PPARγ, its downstream target genes (including PGC1α, NRF-1 and Tfam) and mitochondrial function in mHtt expressing N2A cells. Rosiglitazone treatment also significantly reduced mHtt aggregates that included ubiquitin (Ub) and heat shock factor 1 (HSF1), as assessed by a filter-retardation assay, and increased the levels of the functional ubiquitin-proteasome system (UPS), HSF1 and heat shock protein 27/70 (HSP27/70) in N2A cells. Moreover, rosiglitazone treatment normalized endoplasmic reticulum (ER) stress sensors Bip, CHOP and ASK1, and significantly increased N2A cell survival. Taken together, these findings unveil new insights into the mechanisms by which activation of PPARγ signaling protects against the HD-mediated neuronal impairment. Further, our data also support the concept that PPARγ may be a novel therapeutic target for treating HD.

Leaf‐derived cecidomyiid galls are sinks in Machilus thunbergii (Lauraceae) leaves

Three relevant hypotheses - nutrition, environment and the enemies hypothesis - often invoked to explore source and sink relationships between galls and their host plants are still under dispute. In this research, chlorophyll fluorescence, gas exchange capacity, stomatal conductance, total carbon and nitrogen, total soluble sugars and starches, and scanning and transmission electron microscopy of two types of galls were used to investigate source-sink relationships. Compared with host leaves, these galls demonstrated slightly lower chlorophyll fluorescence; however, gas exchange capacity and stomatal conductance were not detected at all. Scanning electron micrographs demonstrated that the abaxial epidermis of host leaves contain normal amounts of stomata, whereas no stomata were observed on the exterior and interior surfaces of both types of galls. In addition, gall inner surfaces were covered with many kinds of fungal hyphae. Gall total carbon (C) and nitrogen (N) levels were lower but the C/N ratio was higher in galls than host leaves. Both types of galls accumulated higher total soluble sugars and starches than host leaves. Transmission electron micrographs also revealed that both types of galls contain plastoglobuli and giant starch granules during gall development. Results strongly indicate that leaf-derived cecidomyiid galls are sinks in Machilus thunbergii leaves. However, it is perplexing how larvae cycle and balance CO(2) and O(2) in gall growth chambers without stomata.

Oryza sativa protein phosphatase 1a (OsPP1a) involved in salt stress tolerance in transgenic rice

Serine/threonine protein phosphatases (PPs) can be grouped into PP1 and PP2 based on enzymological criteria using specific inhibitors and activators. PP2 receives abscisic acid as signal and negative regulation of tolerance of high salt, drought, and cold stresses, yet the role of PP1 in stress tolerance remains unknown. The objective of this study was to transfer OsPP1a cDNA to rice via Agrobacterium tumefaciens strain EHA105 to assess the mechanisms by which it can confer tolerance to salt treatment. All OsPP1a transcript levels except for OsPP1a-4 detected in transgenic lines were significantly higher than in non-transgenic (NT) plants. Transgenic plants overexpressing OsPP1a showed enhanced tolerance to high salt treatment, SnRK1A, and two stress-responsive genes, OsNAC5 and OsNAC6, which were up-regulated in transgenic OsPP1a-2, OsPP1a-3, and OsPP1a-6 lines. The gene expression profiles of lines OsPP1a-2, -3, and -6 were well-matched with the data for ascorbate peroxidase (APX) and superoxide dismutase (SOD) activity, scavenging the DPPH radical, and malondialdehyde content in NT and transgenic plants under salt stress treatment. In addition, transgenic rice plants also exhibited higher survival rates and plant heights, fewer oxidative injuries, and grew faster than NT plants exposed to salt treatment. Thus, the overexpression of OsPP1a in rice may be useful for enhancing tolerance in high-salt areas.