Phenolic compounds affect intracellular free $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) signaling. The study examined whether the simple phenolic compound octyl gallate affects ATP-induced $Ca^{2+}$ signaling in PC12 cells using fura-2-based digital $Ca^{2+}$ imaging and whole-cell patch clamping. Treatment with ATP ($100\;{\mu}M$) for 90 s induced increases in $[Ca^{2+}]_i$ in PC12 cells. Pretreatment with octyl gallate (100 nM to $20\;{\mu}M$) for 10 min inhibited the ATP-induced $[Ca^{2+}]_i$ response in a concentration-dependent manner ($IC_{50}=2.84\;{\mu}M$). Treatment with octyl gallate ($3\;{\mu}M$) for 10 min significantly inhibited the ATP-induced response following the removal of extracellular $Ca^{2+}$ with nominally $Ca^{2+}$-free HEPES HBSS or depletion of intracellular $Ca^{2+}$ stores with thapsigargin ($1\;{\mu}M$). Treatment for 10 min with the L-type $Ca^{2+}$ channel antagonist nimodipine ($1\;{\mu}M$) significantly inhibited the ATP-induced $[Ca^{2+}]_i$ increase, and treatment with octyl gallate further inhibited the ATP-induced response. Treatment with octyl gallate significantly inhibited the $[Ca^{2+}]_i$ increase induced by 50 mM KCI. Pretreatment with protein kinase C inhibitors staurosporin (100 nM) and GF109203X (300 nM), or the tyrosine kinase inhibitor genistein ($50\;{\mu}M$) did not significantly affect the inhibitory effects of octyl gallate on the ATP-induced response. Treatment with octyl gallate markedly inhibited the ATP-induced currents. Therefore, we conclude that octyl gallate inhibits ATP-induced $[Ca^{2+}]_i$ increase in PC12 cells by inhibiting both non-selective P2X receptor-mediated influx of $Ca^{2+}$ from extracellular space and P2Y receptor-induced release of $Ca^{2+}$ from intracellular stores in protein kinase-independent manner. In addition, octyl gallate inhibits the ATP-induced $Ca^{2+}$ responses by inhibiting the secondary activation of voltage-gated $Ca^{2+}$ channels.
To investigate whether caffeic acid phenethyl ester (CAPE) could affect cancer cell viabilities and gene expression, human colorectal HCT116 cells were incubated with CAPE. CAPE decreased cancer cell viabilities and induced apoptosis in a dose-dependent manner. To analyse differently expressed genes by CAPE, we performed oligo DNA microarray analysis. We found that 266 genes were up-regulated more than twofold, whereas 143 genes were down-regulated more than twofold by 24 hr of treatment with $20{\mu}M$ CAPE. Among the up-regulated genes, we selected 3 genes (NSAID activated gene-1 [NAG-1], cyclin-dependent kinase inhibitor 1A [CDKN1A, p21] and growth arrest and DNA-damage-inducible alpha [GADD45A]) and performed reverse-transcription PCR to confirm microarray data. In addition, we found that CAPE increased NAG-1 gene and NAG-1 protein expression in a dose-dependent manner. And, several other phytochemicals (resveratrol, genistein, daidzein and capsaicin) also could induce NAG-1 expression in human colorectal HCT116 cells. However, CAPE was the highest inducer of NAG-1, even in low concentrations. Overall, these results imply that cancer cell death by CAPE is closely related with over-expression of NAG-1.
Inhibitors of EGFR (epidermal growth factor receptor) kinase activity may prove useful to therapeutically intervene in cancer and to treat other proliferative diseases. In this study, we investigated the inhibitive effects of two compounds named 63013 and 63033 possess a [1,4]-dioxino quinazoline structure that links the alkoxy side chains together and their structural characteristics are considered to allow better solubility than the dialkoxyquinazoline derivatives. The EGFR kinase activities of A431 human epidermoid carcinoma cells, stimulated by EGF were inhibited by treatment with 63013 and 63033 in a dose-dependent manner respectively. Consistent with the compound-mediated EGFR kinase suppression, the major EGF-related downstream target molecules, such as MEK1/2, MAPK p44/42, AKT and STAT3, were also suppressed by both compounds. Interestingly, both compounds led to cell growth inhibition at a lower concentration than that of Gefitinib (Iressa$^{(R)}$). Collectively, our study showed that both compounds may have good therapeutic potential as an EGFR kinase specific inhibitor to treat EGFR-related diseases.
Purpose: The purpose of this study was to ascertain whether radiation adaptive response could be induced by high dose I-131 therapy in patients with differentiated thyroid cancer. Materials and Methods: Lymphocytes from 21 patients (7 males, 14 females, mean age $55{\pm}12$ years) were collected before and after administration of 5,550 MBq (150 mCi) I-131. They were exposed to a challenge dose of 1 Gy gamma rays using a Cs-137 cell irradiator. The number of ring-form (R) and dicentric (D) chromosomes was counted under the light microscope, and used to calculate the frequency of chromosomal aberration. Ydr, which was defined as the sum of R and D divided by the total number of counted lymphocytes. Results: Ydr in patients before I-131 therapy ($0.09{\pm}0.01$) was not different from that of controls ($0.08{\pm}0.01$). Ydr was significantly increased to $0.13{\pm}0.02$ (p<0.0001) after I-131 therapy. Increase of Ydr after the challenge irradiation of 1 Gy was significantly lower in patients after I-131 therapy than before I-131 therapy ($0.17{\pm}0.03\;vs\;0.21{\pm}0.02$, p<0.0001). Cycloheximide (CHM), an inhibitor of protein synthesis, abolished this effect. Ydr after CHM ($0.20{\pm}0.01$) was significantly higher than Ydr after I-131 therapy ($0.17{\pm}0.03$, p<0.0001), but was not different from Ydr before I-131 therapy ($0.21{\pm}0.02$).Conclusion: High dose I-131 therapy induces an adaptive response in peripheral lymphocytes of patients with well-differentiated thyroid cancer, which is associated with protein synthesis.
Quan, He Xiu;Kim, Sun-Young;Jin, Xuan-Shun;Park, Jong-Kwan;Kim, Sung-Zoo;Cho, Kyung-Woo
The Korean Journal of Physiology and Pharmacology
/
v.10
no.3
/
pp.149-154
/
2006
Selective inhibition of phosphodiesterase (PDE) 5 opened a new therapeutic approach for cardiovascular disorders. Therefore, the effect of PDE5 inhibition on the cardiac function should thoroughly be defined. The purpose of the present study was to define the effects of sildenafil, a selective inhibitor of PDE5, on the atrial cGMP efflux, atrial dynamics, and the release of atrial natriuretic peptide (ANP). By perfusing rabbit left atria to allow atrial pacing, changes in atrial stroke volume and pulse pressure, transmural extracellular fluid translocation, cGMP efflux, and ANP secretion were measured. SIN-I, an NO donor and soluble (s) guanylyl cyclase (GC) activator, and C-type natriuretic peptide (CNP), an activator of particulate (p) GC activator, were used. Sildenafil increased basal levels of cGMP efflux slightly but not significantly. Sildenafil in a therapeutic dose increased atrial dynamics (for atrial stroke volume, $2.84{\pm}1.71%$, n=12, vs $-0.71{\pm}0.86%$, n=21; p<0.05) and decreased ANP release ($-9.02{\pm}3.36%$, n=14, vs $1.35{\pm}3.25%$, n=23; p < 0.05), however, it had no effect on the SIN-1- or CNP-induced increase of cGMP levels. Furthermore, sildenafil in a therapeutic dose accentuated SIN-1-induced, but not CNP-induced, decrease of atrial pulse pressure and ANP release. These data indicate that PDE5 inhibition with sildenafil has a minor effect on cGMP levels, but has a distinct effect on pGC-cGMP- and sGC-cGMP-induced contractile and secretory function.
It has been reported that the luteal function may be regulated by the intracellular $Ca^{++}$ level which may be adjusted partially by the high affinity $Ca^{++}-ATPase$ in luteal cell membranes. Then, one may expect that luteotropic and/or luteolytic agents, such as gonadotropins, prostaglandin $F_{2{\alpha}}\;(PGF_{2{\alpha}})$ and ouabain, affect the intracellular $Ca^{++}$ level. In this present study, therefore, we examined the effects of luteinizing hormone (LH, or human chorionic gonadotropin, hCG), $PGF_{2{\alpha}}$ and ouabain on the kinetic properties of the high affinity $Ca^{++}-ATPase$ in light membrane, heavy membrane, and microsomal fractions from the highly luteinized ovary. LH (or hCG) increased the affinity and the Vmax for $Ca^{++}$ both in light membrane and heavy membrane. $PGF_{2{\alpha}}$ increased the Vmax in light membrane and decreased the Km in heavy membrane for $Ca^{++}$ at low concentration $(5\;{\mu}g/ml)$. At higher concentration, however, $PGF_{2{\alpha}}$ oppositly affected on kinetic properties, that shown at low concentration. Ouabain, a potent inhibitor of $Na^+-K^+-ATPase$, increased the Km at high concentration $(10^{-4}\;M)$, however, decreased the Vmax for $Ca^{++}$ in light membrane at low concentration $(10^{-6}\;M)$. Also, ouabain increased the Km for $Ca^{++}$ in heavy membrane without changes in the Vmax at both concentrations. It seems that LH and low dose of $PGF_{2{\alpha}}$ increase the intracellular $Ca^{++}$ level and cause in activation of $Ca^{++}-ATPase$, however, higher dose of $PGF_{2{\alpha}}$ and ouabain inhibit directly $Ca^{++}-ATPase$ activity and result in increase in intracellular $Ca^{++}$ level. According to the above results, we suggest that luteotropic and/or luteolytic agents regulate the luteal progesterone $(P_4)$ production through two different pathways; one is cyclic adenosine monophosphate (cAMP)-dependent and another is $Ca^{++}-dependent$. Intracellula. $Ca^{++}$ level regulated by the high affinity $Ca^{++}-ATPase$ may affect both pathways in a time-dependent fashion. LH (or hCG) acts on the luteal $P_4$ production via both pathways. The initial step is $Ca^{++}$ dependent, and the late step is cAMP dependent. $PGF_{2{\alpha}}$ and ouabain increase the intracellular $Ca^{++}$ concentration so that basal luteal $P_4$ production is increased and LH-stimulated $P_4$ production is inhibited by the inhibiting LH-dependent adenylate cyclase activity.
Zhang, Liying;Li, Defa;Qiao, Shiyan;Wang, Jituan;Bai, Lu;Wang, Zongyi;Han, In K.
Asian-Australasian Journal of Animal Sciences
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v.14
no.11
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pp.1598-1604
/
2001
Eight $12.4{\pm}0.6kg$ initial body weight crossbred barrows were used to determine the effect of soybean galactooligosaccharides on nutrient and energy digestibility, and digesta transit time. Four dietary treatments were utilized in this trial. Treatment one was a corn-soybean meal based diet (SBM) containing raffinose and stachyose at the levels of 0.16% and 0.75%, respectively. Treatment two (control) was a corn-HP300 (soybean concentrate protein) diet. In treatments three and four, 1.1% and 2.2% commercial stachyose was added to the control diet to provide total dietary stachyose at the levels of 1% and 2%, respectively. The soybean galactooligosaccharides (raffinose + stachyose) level in treatment one was slightly lower compared to that in treatment three. Three collection periods were run with two pigs for each treatment/period. There was a 4 d adjustment period followed by a 3 d collection period. The results showed that the nitrogen retention (86.79%) of pigs fed treatment two diet was higher than that of pigs fed treatment one by 5.2% (p<0.05). The nitrogen retention of treatment three was intermediate 83.09%. The apparent fecal digestibility of all amino acids in treatment two was numerically highest, followed by treatments three and four. However, there were no significant difference among groups (p>0.05). The dry matter (DM), organic matter (OM), crude protein (CP), and crude fiber (CF) digestibility numerically decreased as the soybean galactooligosaccharides level increased, but were not significantly different (p>0.05). Chromium content in feces (from the inclusion of 0.3% chromic oxide in the diets) differed among treatments (p<0.05) at 15 h, 18 h, and 21 h after eating. This showed that the digesta transit time was differed significantly among treatments. Treatment four was the shortest, followed by treatment three, SBM and control. The results demonstrated that in the absence of antinutritional factors and soybean antigen protein, inclusion of 1% and 2% stachyose in corn-HP300 diet has no significant effect on the digestibility of DM, OM, CP, CF and amino acids. When the soybean galactooligosaccharide level in diet one and diet three were adjusted to be almost the same, antinutritional factors such as trypsin inhibitor and soybean antigen protein could decrease the nutrient digestibility and nitrogen retention rate of diet. High levels of soybean galactooligosaccharides shortened the digesta transit time in the intestinal tract. This trial suggested that the total level of soybean galactooligosaccharides (stachyose+raffinose) in the weanling piglet diet is better not to exceed 1% when common soybean meal is used as main protein source.
Kim, Soo-Kyung;Kang, Hee-Kyoo;Jun, Jin-Hyun;Choi, Kyoo-Wan;Kim, Moon-Kyoo
Development and Reproduction
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v.5
no.1
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pp.17-21
/
2001
This study was conducted to investigate the expression pattern of Trypsin-like enzyme and the effect of a trypsin inhibitor(benzimidine) on hatching process during in-vitro culture of mouse preimplantation embryos. The Trypsin-like enzyme was identified by rhodamine-conjugated Trypsin substrate probe. The expression of trypsin-like enzyme was firstly detected at the late morula stage, and the enzyme was uniformly localized in the trophectoderm of late blastocysts. Especially, intense fluorescence was observed in the blebbing area of hatching blastocysts. Bisbenzamidine, contained in culture media, did not alter embryonic development from 4-cell stage to the expanded blastocyst but decrease the hatching rate in ImM concentration (15.8% vs 89.7%, p<0.02). In the treatment of bisbenzimidine (5mM) for 12 hours according to the embryonic stage of mouse, the hatching rate of control (83.0%) and treatment in late blastocysts (8.7%) were significantly (p<0.01) different. From these results, we suggested that the hatching enzyme having trypsin-like activity was localized from the late morula stage, and the hatching process by this enzyme was activated in the late blastocyst stage of mouse embryos.
Shin, Dong Yeok;Kang, Ho Sung;Bae, Song-Ja;Jung, Jee H.;Choi, Yung Hyun
Journal of Marine Bioscience and Biotechnology
/
v.1
no.2
/
pp.63-70
/
2006
Natural product compounds are the source of numerous therapeutic agents. The marine environment produces natural products from a variety of structural classes exhibiting activity against numerous disease targets including anticancer agents. Among these, pectenotoxin-2 (PTX-2), which was first identified as a cytotoxic entity in marine sponges, which depolymerizes actin filaments, was found to be highly effective and more potent to activate an intrinsic pathway of apoptosis in p53-deficient tumor cells compared to those with functional p53 both in vitro and in vivo. However, the anti-proliferative mechanism of the compound at non-cytotoxic concentrations has not yet been explored. In the current study, we sought to investigate anti-proliferation and apoptosis of PTX-2 against U937 human leukemic cells and its underlying molecular mechanism. Exposure of U937 cells to PTX-2 resulted in growth inhibition and induction of apoptosis in dose- and time-dependent manner as measured by MTT assay, fluorescent microscopy and flow cytometric analysis. The anti-proliferative effect of PTX-2 was associated with a marked increase in the expression of cyclin-dependent kinase p21 (WAF1/CIP1) mRNA which was tumor suppressor p53-independent. The increase in apoptosis was connected with a time-dependent down-regulation of anti-apoptotic Bcl-XL and inhibitor of apoptosis proteins (IAPs) family such as XIAP and cIAP-2. Though additional studies are needed, these findings suggested that PTX-2-induced inhibition of U937 cells was associated with the induction of apoptotic cell death and the results provided important new insights into the possible molecular mechanisms of the anti-cancer activity of PTX-2.
This study was performed to investigate the effect of essential oils and ethanolic extracts of approximately 650 plant species on acetylcholine esterase (AChE) enzyme activity using Ellman's colorimetric method in 96-well microplates. The results showed that the ethanolic extracts from twig of Sophora subprostrata, twig of Phellodendron amurense, seed of Corylopsis coreana, and essential oil (EO) from Citrus paradisi, Cupressus sempervirens, Ocimum basilicum, Pinus sylvestris and Rosmarinus officinalis inhibited more than 80% of AChE activity. Among these, EO from Pinus sylvestris, C. sempervirens and C paradisi exhibited higher values of AChE inhibitory activity, which were 75, 84 and 99% at a concentration of 50 ug/ml, respectively. Finally, EO from C paradisi (grapefruit, GEO) showed the highest inhibitory activity towards AChE, which showed 91% of inhibition at a concentration of 20 ug/ml. We also examined the anti-dementia effects of GEO in mouse by passive avoidance test and Morris water maze test. The model mouse (male, ICR) of dementia (negative control) was induced by administration of scopolamine (1 mg/kg body weight). The latency time of sample group administrated with GEO (100 mg/kg, p.o.) increased significantly as compared with negative control on passive avoidance test. There were significant recovery from the scopolamine-induced deficits on learning and memory in water maze test through daily administrations with GEO (100 mg/kg, p.o.). From these results, we conclude that GEO treatment might enhance the cognitive function, suggesting that the EO of C. paradis may be a potential candidate for improvement of perceptive ability and dementia.
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