Hye-Jung Kim

QIGONG REDUCED BLOOD PRESSURE AND CATECHOLAMINE LEVELS OF PATIENTS WITH ESSENTIAL HYPERTENSION

This study was designed to investigate the efficacy of Qigong as a non-pharmacological treatment of hypertension and evaluate the contribution of Qigong in the blood pressure (BP) reduction of essential hypertension patients. Fifty-eight patients volunteered to participate in this study and were randomly divided into either a Qigong group (n = 29), or a wait list control group (n = 29). In response to 10 weeks of Qigong, systolic blood pressure (SBP), diastolic blood pressure (DBP), and rate pressure product (RPP) were decreased significantly. There was a significant reduction of norepinephrine, epinephrine, cortisol, and stress level by the Qigong. These results suggest that Qigong may reduce BP and catecholamines via stabilizing the sympathetic nervous system. Therefore, Qigong is an effective nonpharmacological modality to reduce BP in essential hypertensive patients

Evidence that Cisplatin-induced Auditory Damage is Attenuated by Downregulation of Pro-inflammatory Cytokines Via Nrf2/HO-1

Recently, we demonstrated that pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 played a critical role in cisplatin-induced cochlear injury and that flunarizine, known as a T-type Ca2+ channel antagonist, induced a cytoprotective effect against cisplatin cytotoxicity in HEI-OC1 cells by the activation of NF-E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) cascade through PI3K-Akt signaling but calcium-independent pathway. We report here that flunarizine markedly attenuates cisplatin-induced pro-inflammatory cytokine secretion and their messenger RNA transcription as well as cisplatin cytotoxicity through the activation of Nrf2/HO-1 and downregulation of NF-κB. In HEI-OC1 cells, overexpression of Nrf2/HO-1 by gene transfer or pharmacological approaches attenuated cisplatin-induced cytotoxicity and pro-inflammatory cytokine production. On the contrary, inhibition of Nrf2/HO-1 signaling by pharmacological inhibitors or specific small interfering RNAs significantly abolished the beneficial effects of flunarizine. Flunarizine also attenuated cisplatin-mediated MAPK activation and pharmacological inhibition of MAPKs, especially MEK1/ERK, blocked cisplatin-induced NF-κB activation in HEI-OC1 cells. Furthermore, WT-Nrf2 overexpression effectively blocked MAPK activation after cisplatin exposure. Finally, orally administrated Sibelium™, the trade name of flunarizine, suppressed the increase of pro-inflammatory cytokines by cisplatin in both serum and cochleas of mice, whereas it increased HO-1 expression in cochleas. These results indicate that flunarizine induces a protective effect against cisplatin ototoxicity through the downregulation of NF-κB by Nrf2/HO-1 activation and the resulting inhibition of pro-inflammatory cytokine production in vitro and in vivo.

EFFECTS OF QIGONG ON BLOOD PRESSURE, HIGH-DENSITY LIPOPROTEIN CHOLESTEROL AND OTHER LIPID LEVELS IN ESSENTIAL HYPERTENSION PATIENTS

This study investigated the effectiveness of Qigong on blood pressure and several blood lipids, such as high-density lipoprotein (HDL) cholesterol, Apolipoprotein A1 (APO-A1), total cholesterol (TC), and triglycerides (TG) in hypertensive patients. Thirty-six patients were randomly divided into either the Qigong group, or a wait-listed control group. Blood pressures decreased significantly after eight weeks of Qigong. The levels of TC, HDL, and APO-A1 were changed significantly in the Qigong group post-treatment compared with before treatment. In summary. Qigong acts as an antihypertensive and may reduce blood pressure by the modulation of lipid metabolism.

Hibiscus Extract Inhibits the Lipid Droplet Accumulation and Adipogenic Transcription Factors Expression of 3T3-L1 Preadipocytes

OBJECTIVES This study was designed to investigate the effect of hibiscus (Hibiscus sabdariffa) on adipogenic differentiation of 3T3-L1 cells at the cellular and molecular levels. DESIGN Various concentrations of hibiscus extract were added to confluent 3T3-L1 preadipocytes at the outset of the differentiation program and further incubated for 36 hours. Cells were maintained in postdifferentiation medium containing insulin with hibiscus extract in complete culture medium. RESULTS Hibiscus extract inhibited the adipocyte differentiation of 3T3-L1 preadipocytes induced by insulin, dexamethasone, and isobutylmethylxanthine (IBMX) in a dose-dependent manner. Hibiscus blocked the cytoplasmic lipid accumulation when administered at the onset of differentiation and 4 days after induction of differentiation. The inhibitory effect of hibiscus on adipogenic lipid accumulation of preadipocytes was significant (p < 0.01) between control cells and cells treated with hibiscus. Hibiscus extract significantly attenuated the expression of key adipogenic transcription factors, including CCAAT element binding protein (C/EBP)alpha and peroxisome proliferator-activated receptor (PPAR)gamma at protein levels. CONCLUSION These results suggest that hibiscus extract blocks adipogenesis, in part, by its suppression on the expression of adipogenic transcription factors, including C/EBPalpha and PPARgamma.

Leucine-Rich Repeat Kinase 2 (LRRK2) phosphorylates p53 and induces p21(WAF1/CIP1) expression.

BackgroundLeucine-rich repeat kinase 2 (LRRK2) is a gene in which a mutation causes Parkinson’s disease (PD), and p53 is a prototype tumor suppressor. In addition, activation of p53 in patient with PD has been reported by several studies. Because phosphorylation of p53 is critical for regulating its activity and LRRK2 is a kinase, we tested whether p53 is phosphorylated by LRRK2.ResultsLRRK2 phosphorylates threonine (Thr) at TXR sites in an in vitro kinase assay, and the T304 and T377 were identified as putative phosphorylated residues. An increase of phospho-Thr in the p53 TXR motif was confirmed in the cells overexpressing G2019S, and human induced pluripotent stem (iPS) cells of a G2019S carrier. Interactions between LRRK2 and p53 were confirmed by co-immunoprecipitation of lysates of differentiated SH-SY5Y cells. LRRK2 mediated p53 phosphorylation translocalizes p53 predominantly to nucleus and increases p21WAF1/CIP1 expression in SH-SY5Y cells based on reverse transcription-polymerase chain reaction and Western blot assay results. The luciferase assay using the p21WAF1/CIP1 promoter-reporter also confirmed that LRRK2 kinase activity increases p21 expression. Exogenous expression of G2019S and the phosphomimetic p53 T304/377D mutants increased expression of p21WAF1/CIP1 and cleaved PARP, and cytotoxicity in the same cells. We also observed increase of p21 expression in rat primary neuron cells after transient expression of p53 T304/377D mutants and the mid-brain lysates of the G2019S transgenic mice.Conclusionp53 is a LRRK2 kinase substrate. Phosphorylation of p53 by LRRK2 induces p21WAF1/CIP1 expression and apoptosis in differentiated SH-SY5Y cells and rat primary neurons.

GAMMA-INTERFERON (IFN-γ) AUGMENTS APOPTOTIC RESPONSE TO MISTLETOE LECTIN-II VIA UPREGULATION OF FAS/FAS L EXPRESSION AND CASPASE ACTIVATION IN HUMAN MYELOID U937 CELLS

Mistletoe lectin-II, a major composition of Korean mistletoe (Viscum album coloratum), is known as a potent apoptosis inducer. The previous research has demonstrated that Korean mistletoe lectin-II induces apoptosis via c-Jun N terminal kinase (JNK) activation in human myeloid U937 cells. The purpose of this research is to prove the synergistic action of mistletoe lectin-II and interferon-γ (IFN-γ) in the apoptotic cytotoxicity of U937. When U937 cells were treated with mistletoe lectin-II after being differentiated by IFN-γ, the proteolytic activity of caspase-3 and 9 was markedly elevated and that of caspase-8 was prolonged for 18 hr. The activation of caspase-3-like protease requires the earlier cleavage of poly(ADP-ribose) polymerase(PARP). Caspase-1 was, however, not activated during the resting phase and nor in IFN-γ-differentiated U937 cells. Western blot analysis revealed that, in IFN-γ-differentiated U937 cells, the expression of Fas (CD95/APO-1) & Fas ligand(FasL) increases the apoptotic sensitivity against Mistletoe lectin-II. Fas (CD95/APO-1) & FasL were not significantly induced solely by mistletoe lectin-II. Furthermore the activity of JNK1 in U937 cells was also markedly increased with IFN-γ-differentiation, compared to that of the control. These results suggest that the IFN-γ-differentiation of U937 cells increases the susceptibility to mistletoe lectin-II-induced apoptosis.

EFFECT OF MULTI-FUNCTIONAL FABRIC ON SLEEP STAGES AND GROWTH HORMONE LEVELS DURING SLEEP

Nine young girls participated in cross-over sessions, sleeping with either multi-functional fabric (experimental session) or cotton (control session). The relative duration of slow-wave sleep (SWS) was 1.89-fold higher in the experimental session than in the control session. The peak growth hormone (GH) secretion in the experimental session was more than 2.4-fold higher than during the control session (p <. 001). The quality of sleep during the experimental session was significantly better than in the control session (p <. 01). These results suggest that multi-functional fabric wear is effective in inducing deep sleep, increasing GH, and improving the quality of sleep.

Effects of multifunctional fabrics on cardiac autonomic tone and psychological state.

Heart rate variability was compared in 20 subjects wearing multifunctional fabric (experimental sessions) and cotton (control sessions) clothing.- Anxiety, depression, fatigue, and stress levels were lower and emotional levels were higher during the experimental sessions than in the control sessions. Multifunctional fabrics reduced the low-frequency/high-frequency power ratio of heart rate variability. These results support the hypothesis that multifunctional fabrics increase cardiac parasympathetic tone. In addition, subjects had lower heart rates during the experimental sessions compared with controls, suggesting a stabilizing effect on the autonomic nervous system. In conclusion, multifunctional fabrics may act to stabilize both the autonomic nervous system and psychological state.

Protective effects of Debo on zinc-induced apoptosis of C6 glial cells via modulation of intracellular antioxidant, reduced glutathione.

In the present study, the mechanical basis of a traditional herbal prescription, Debo, on cytotoxic damage of the brain cells including C6 glial and PC12 cells has been studied. Traditionally, Debo has been employed for the purpose of preventing responses to trauma, ischemia, and other diseases in the nervous system. C6 glial cells were exposed to oxidative stress through the imployment of ZnCl2, and generates H2O2 and hydroxyl radicals by fenton reaction. ZnCl2-induced death of C6 glial cells, which was revealed as apoptosis by chromatin condensation as well as DNA fragmentation. Pretreatment of Debo significantly prevented apoptotic death of C6 glial cells via inhibition of H2O2 generation as well as the recovering of an antioxidant, reduced glutathione (GSH). Also, deprivation of serum and glucose, found in ischemia, deceased the viability of PC12 cells up to 60% via generation of H2O2. However, Debo significantly protected cells from ischemic damage through decrease in H2O2 generation. Furthermore, Debo markedly inhibited the transcriptional activation of NF-κB by ZnCl2 in C6 glial cells. These results suggest that Debo may function as an antioxidant system against free radicals and be applicable to protect brain cells against oxidative or ischemic stresses.

External Qi therapy to treat symptoms of Agent Orange Sequelae in Korean combat veterans of the Vietnam War.

We investigated the efficacy of Qi therapy as a non-pharmacological treatment for various symptoms presented by Korean combat veterans of the Vietnam War with Agent Orange Sequelae. Nine subjects volunteered to receive 30 minutes of Qi therapy, twice per day for 7 days. There was marked improvement in 89% of the patients with impaired physical activity, 86% of those with psychological disorder, 78% of those with heavy drug use, and 67% of those with fatigue, indigestion and high blood glucose levels. This data suggests that Qi therapy combined with conventional treatment has positive effects in reducing and managing the pain, psychosomatic disorders, and substance abuse in patients with Agent Orange Sequelae. We cannot completely discount the possible influence of the placebo effect, and more objective, clinical measures are needed to study the long-term effects of Qi therapy.