Albanin A, Derived from the Root Bark of Morus alba L., Depresses Glutamate Release in the Rat Cerebrocortical Nerve Terminals via Ca2+/Calmodulin/Adenylate Cyclase 1 Suppression

Yi Chang,Chi-Feng Hung,Horng Huey Ko,Su-Jane Wang 한국식품영양과학회 2021 Journal of medicinal food Vol.24 No.3

Decreasing synaptic release of glutamate may counteract glutamate excitotoxicity in many neurological diseases. In this study, we investigated the effect of albanin A, a constituent in the root bark of Morus alba L., on the release of glutamate in rat cerebral cortex nerve endings (synaptosomes). We found that albanin A at 5–30μM suppressed 4-aminopyridine (4-AP)-induced release of glutamate. This phenomenon was abolished by extracellular calcium removal or by vesicular transporter inhibition, and was associated with a decrease in intrasynaptosomal Ca2+ levels. However, albanin A had no effect on the synaptosomal membrane potential. The inhibition of N- and P/Q-type Ca2+ channels, calmodulin, adenylate cyclase (AC), and protein kinase A, abolished the effect of albanin A on the glutamate release evoked by 4-AP. Moreover, the albanin A-mediated inhibition of glutamate release was prevented by the Ca2+/calmodulin-stimulated AC1 inhibitor. Western blot showed that AC1, but not AC8, was presented in the synaptosomes, and albanin A reduced 4-AP-induced increases in synaptosomal cyclic adenosine monophosphate content. In addition, albanin A pretreatment substantially attenuated neuronal damage in a rat model of kainic acid-induced glutamate excitotoxicity. Our data reveal that albanin A suppresses glutamate release by decreasing Ca2+/calmodulin/AC1 activation in synaptosomes and exerts neuroprotective effect in vivo.

Long-term Care Nurses’ Communication Difficulties with People Living with Dementia in Taiwan

Jing-Jy Wang,Pei-Fang Hsieh,Chi-Jane Wang 한국간호과학회 2013 Asian Nursing Research Vol.7 No.3

Purpose: Impairments in word finding, language skills and memory in dementia patients increase the obstacles for health professionals to provide effective care. Although some research on communication with dementia patients has been done, no research that pre-assessed nurses’ difficulties in communicating with dementia patients has been identified. This study aims to explore nurses’ difficulties in communicating with patients who have dementia. Methods: This was a qualitative research using the phenomenological approach. Data were collected through in-depth interviews. Fifteen nurses with at least 6 months of dementia care experience participated in this study. Each interview was audio-taped and transcribed within 48 hours after each interview. Participants were asked to respond to the question, “Please describe the difficulties in communicating with patients who have dementia.”Results: Through content analysis, two themes, each with two subthemes emerged: Different language, including repetitive responses and lack of language consensus; blocked messages, including difficulty in accessing emotions and in understanding needs. Ineffective language refers to a lack of agreement dialect between the nurse and the patient while blocked messages refer to the inability of nurses to understand the true underlying meaning of messages the patients send out through verbal or nonverbal behaviors or expression. Conclusion: The results can serve as reference for planning dementia communication education for school curriculum to enhance student nurses’ communication abilities and for junior nurses working in long-term or acute care settings to increase nurses’ patient-centered communication abilities with the ultimate goal of improving quality of care for patients with dementia.

Eupafolin Suppresses P/Q-Type Ca²⁺ Channels to Inhibit Ca²⁺/ Calmodulin-Dependent Protein Kinase II and Glutamate Release at Rat Cerebrocortical Nerve Terminals

( Anna Chang ),( Chi-Feng Hung ),( Pei-Wen Hsieh ),( Horng-Huey Ko ),( Su-Jane Wang ) 한국응용약물학회 2021 Biomolecules & Therapeutics(구 응용약물학회지) Vol.29 No.6

Eupafolin, a constituent of the aerial parts of Phyla nodiflora, has neuroprotective property. Because reducing the synaptic release of glutamate is crucial to achieving pharmacotherapeutic effects of neuroprotectants, we investigated the effect of eupafolin on glutamate release in rat cerebrocortical synaptosomes and explored the possible mechanism. We discovered that eupafolin depressed 4-aminopyridine (4-AP)-induced glutamate release, and this phenomenon was prevented in the absence of extracellular calcium. Eupafolin inhibition of glutamate release from synaptic vesicles was confirmed through measurement of the release of the fluorescent dye FM 1-43. Eupafolin decreased 4-AP-induced [Ca²⁺]_i elevation and had no effect on synaptosomal membrane potential. The inhibition of P/Q-type Ca²⁺ channels reduced the decrease in glutamate release that was caused by eupafolin, and docking data revealed that eupafolin interacted with P/Q-type Ca²⁺ channels. Additionally, the inhibition of calcium/calmodulindependent protein kinase II (CaMKII) prevented the effect of eupafolin on evoked glutamate release. Eupafolin also reduced the 4-AP-induced activation of CaMK II and the subsequent phosphorylation of synapsin I, which is the main presynaptic target of CaMKII. Therefore, eupafolin suppresses P/Q-type Ca²⁺ channels and thereby inhibits CaMKII/synapsin I pathways and the release of glutamate from rat cerebrocortical synaptosomes.

The Indonesian Version of the Exercise Self-Efficacy Scale: Cross-cultural Adaptation and Psychometric Testing

Hakim Arif R.,Wang Shan-Tair,Widiantoro Fransiskus X.,Hannan Mujib,Wang Chi-Jane,Fetzer Suzan J. 한국간호과학회 2020 Asian Nursing Research Vol.14 No.5

Purposes: The study aimed to translate the Exercise Self-Efficacy Scale (ESES) into Indonesian and test the cultural equivalence, reliability, and validity of the new version for university students. Methods: The cross-sectional study recruited 379 Indonesian university students using convenience sampling. Phase 1, a culturally appropriate version of the ESES was developed in the Indonesian language. Phase 2, the psychometric properties were determined through exploratory factor analysis, bootstrap factor analysis, and confirmatory factor analysis. The internal consistency reliability was tested using Cronbach's a, whereas the stability using intraclass correlation coefficient to assess. Results: The students' ages ranged from 17 to 39 years, and 65.0% were women. For translation equivalence, the mean item content validity indexes ranged from 3.5 to 4, and all items were understandable. The 16-item scale exhibited cross-cultural appropriateness and readability, with a three-factor model explaining 62.3% of the variance in exercise self-efficacy. A bootstrap analysis using 100 resamples further confirmed the three-factor model. The indices of the good-fit model that used the three-factor by two-stage least squares method were satisfactory, with c2/df ¼ 3.3, goodness of fit index = .88, and root mean-square error of approximation = .05 (p < .001). The Cronbach's a was .78, .80, and .92 for factors 1, 2, and 3, respectively. The test–retest reliability was demonstrated with an intraclass correlation coefficient of .91, indicating adequate measurement stability. Conclusion: The 16-item ESES-I has acceptable validity and reliability; however, a broader application of the scale requires further testing in different populations to confirm its external validity.

Allicin Inhibits Glutamate Release from Rat Cerebral Cortex Nerve Terminals Through Suppressing Ca2+ Influx and Protein Kinase C Activity

Cheng Wei Lu,Chi-Feng Hung,Tzu Yu Lin,Ting Yang Hsieh,Su-Jane Wang 한국식품영양과학회 2019 Journal of medicinal food Vol.22 No.7

Evidence indicates that indirect inhibitory regulation of glutamatergic transmission, via reducing glutamate release, may induce neuroprotection. The present work was designed to examine whether allicin, a major component of garlic with neuroprotective effects, affected the release of glutamate evoked by 4-aminopyridine in rat cerebrocortical nerve terminals (synaptosomes). Allicin caused a potent inhibition on the release of glutamate evoked by 4-aminopyridine, and this inhibitory effect was abolished in the presence of Ca2+-free medium and vesicular transporter inhibitor. Allicin decreased the 4-aminopyridine-evoked elevation of intrasynaptosomal Ca2+ levels, but had no effect on the synaptosomal plasma membrane potential. The allicin-mediated inhibition of glutamate release was prevented by the N- and P/Q-type channel blocker and the protein kinase C (PKC) inhibitor, but was not affected by the intracellular Ca2+-release inhibitors, mitogen-activated protein kinase inhibitor, and protein kinase A inhibitor. Western blotting data also showed that allicin significantly reduced the phosphorylation of PKC. Together, these data indicate that in rat cerebrocortical nerve terminals, allicin depresses glutamate release and appears to decrease N- and P/Q-type Ca2+ channel and PKC activity.

Cilostazol ameliorates diabetic nephropathy by inhibiting highglucose-induced apoptosis

Chien-Wen Chian,Yung-Shu Lee,Yi-Ju Lee,Ya-Hui Chen,Chi-Ping Wang,Wen-Chin Lee,Huei-Jane Lee 대한생리학회-대한약리학회 2020 The Korean Journal of Physiology & Pharmacology Vol.24 No.5

Diabetic nephropathy (DN) is a hyperglycemia-induced progressive development of renal insufficiency. Excessive glucose can increase mitochondrial reactive oxygen species (ROS) and induce cell damage, causing mitochondrial dysfunction. Our previous study indicated that cilostazol (CTZ) can reduce ROS levels and decelerate DN progression in streptozotocin (STZ)-induced type 1 diabetes. This study investigated the potential mechanisms of CTZ in rats with DN and in high glucose-treated mesangial cells. Male Sprague-Dawley rats were fed 5 mg/kg/day of CTZ after developing STZ-induced diabetes mellitus. Electron microscopy revealed that CTZ reduced the thickness of the glomerular basement membrane and improved mitochondrial morphology in mesangial cells of diabetic kidney. CTZ treatment reduced excessive kidney mitochondrial DNA copy numbers induced by hyperglycemia and interacted with the intrinsic pathway for regulating cell apoptosis as an antiapoptotic mechanism. In high-glucose-treated mesangial cells, CTZ reduced ROS production, altered the apoptotic status, and down-regulated transforming growth factor beta (TGF-β) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB). Base on the results of our previous and current studies, CTZ deceleration of hyperglycemia-induced DN is attributable to ROS reduction and thereby maintenance of the mitochondrial function and reduction in TGF-β and NF-κB levels.