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Chin J Physiol ; 64(4): 202-209, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34472451


Gamma-linolenic acid (GLA), a natural fatty acid obtained from oils of various vegetables and seeds, has been demonstrated as an anticancer agent. In this work, we investigated the anticancer effects of GLA on breast cancer BT-474 cells. GLA at 30 µM, a concentration reportedly within the range of circulating concentrations in clinical studies, caused apoptotic cell death. GLA caused an elevation in mitochondrial Ca2+ level and a decrease in mitochondrial membrane potential. GLA treatment depleted cyclopiazonic acid (CPA)-sensitive Ca2+ store and triggered substantial Ca2+ influx. Intracellular Ca2+ release triggered by GLA was suppressed by 3 µM xestospongin C (XeC, IP3 receptor-channel blocker) and 100 µM ryanodine (ryanodine receptor-channel blocker), suggesting that the Ca2+ release was via IP3 receptor-channel and ryanodine receptor-channel. Increased expressions of p-eIF2α and CHOP were observed in GLA-treated cells, suggesting GLA-treated cells had increased expressions of p-eIF2α and CHOP, which suggest endoplasmic reticulum (ER) stress. In addition, GLA elicited increased production of reactive oxygen species. Taken together, our results suggest a basal level of GLA induced apoptotic cell death by causing Ca2+ overload, mitochondrial dysfunction, Ca2+ store depletion, ER stress, and oxidative stress. This is the first report to show that GLA caused Ca2+ store depletion and ER stress. GLA-induced Ca2+ store depletion resulted from opening of IP3 receptor-channel and ryanodine receptor-channel.

Neoplasias da Mama , Ácido gama-Linolênico , Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/metabolismo , Cálcio/metabolismo , Retículo Endoplasmático/metabolismo , Feminino , Humanos , Estresse Oxidativo , Ácido gama-Linolênico/metabolismo
BMJ Open ; 10(3): e034202, 2020 03 25.
Artigo em Inglês | MEDLINE | ID: mdl-32213519


OBJECTIVES: The administration of androgen deprivation therapy (ADT) to patients with metastatic prostate cancer might be associated with some adverse effects such as anaemia; however, few studies have been performed in East Asian populations. This study aimed to investigate the association between ADT and iron-deficiency anaemia (IDA) among patients with prostate cancer in a population-based nationwide cohort. DESIGN: Cohort study. SETTING: Taiwan. PARTICIPANTS: Data for the cohort study were retrieved from the Taiwan National Health Insurance Research Database. Propensity score matching was used to select 7262 patients with prostate cancer who received ADT as the study group and 3631 patients who did not receive ADT as the control group. PRIMARY AND SECONDARY OUTCOME MEASURES: This study individually tracked patients over a 3-year study period and identified those who were subsequently diagnosed with IDA following the index date. RESULTS: The incidence rates of IDA in the study and control groups were 1.66 (95% CI CI 1.45 to 1.86) and 1.01 per 100 person-years (95% CI 0.78 to 1.25), respectively. Furthermore, proportional Cox regression revealed an HR of 1.62 (95% CI 1.24 to 2.12) for IDA in the study group after adjusting for patients' age, monthly income, geographic location, residential urbanisation level and incidence of hyperlipidaemia, diabetes, hypertension, coronary heart disease, inflammatory bowel disease, other cancers and gastrointestinal bleeding. CONCLUSION: Compared with its non-use among patients with prostate cancer, ADT use was associated with a higher risk of IDA.

Antagonistas de Androgênios/uso terapêutico , Anemia Ferropriva/epidemiologia , Neoplasias da Próstata/tratamento farmacológico , Neoplasias da Próstata/epidemiologia , Fatores Etários , Idoso , Antagonistas de Androgênios/efeitos adversos , Humanos , Masculino , Pessoa de Meia-Idade , Metástase Neoplásica , Pontuação de Propensão , Neoplasias da Próstata/patologia , Estudos Retrospectivos , Fatores de Risco , Fatores Socioeconômicos , Taiwan/epidemiologia
Am J Chin Med ; 36(4): 685-93, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-18711766


Panax Notoginseng Burk (PN) has been reported to improve blood circulation, as well as learning and memory functions. The purpose of the present study was to investigate the effect of PN on learning and memory functions in chronic cerebral infarct rats. A cerebral infarct animal model was established by blocking the blood flow of both common carotid arteries and right middle cerebral artery for 90 min followed by reperfusion for 4 weeks. PN (0.5 g/kg) was administered orally 3 days per week for 4 weeks, whereas the control group provided bait and water only. The learning and memory functions were estimated by measuring how successful rats were able to negotiate an 8-arm radial maze test; the test was performed after operation once a week for 4 weeks. Finally, the rats were sacrificed and their brains were removed. The brains were sectioned and analyzed for ED1, glial fibrillary acid protein (GFAP), nuclear factor-kappaB, and brain derivative neurotrophin factor (BDNF) and beta-secretase by immunostaining. Cerebral infarct rats given PN were able to successfully navigate the 8-arm radial maze test four weeks after cerebral infarction. PN also increased ED1, BDNF and beta-secretase immunoreactive cells, but did not increase GFAP and NF-kappaB immunoreactive cells. PN attenuated the reduction in learning and memory functions induced by cerebral infarction in cerebral ischemia-reperfusion injured rats; it also increased the amount of activated microglia and BDNF. These data suggest that the effect of PN, at least in part, is closely related to the increase in BDNF that was generated by activated microglia. The effect that PN has on astrocytes, NF-kappaB and beta-secreatase immunoreactive cells requires further study.

Secretases da Proteína Precursora do Amiloide/metabolismo , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Ectodisplasinas/metabolismo , Deficiências da Aprendizagem/prevenção & controle , Transtornos da Memória/prevenção & controle , Panax notoginseng , Traumatismo por Reperfusão/metabolismo , Animais , Infarto Cerebral/tratamento farmacológico , Infarto Cerebral/metabolismo , Infarto Cerebral/patologia , Doença Crônica , Modelos Animais de Doenças , Medicamentos de Ervas Chinesas/uso terapêutico , Proteína Glial Fibrilar Ácida/metabolismo , Masculino , Aprendizagem em Labirinto , NF-kappa B/metabolismo , Fitoterapia , Ratos , Ratos Sprague-Dawley , Traumatismo por Reperfusão/tratamento farmacológico , Traumatismo por Reperfusão/patologia , Fatores de Tempo
Am J Chin Med ; 35(5): 779-91, 2007.
Artigo em Inglês | MEDLINE | ID: mdl-17963318


The Baihui acupoint has three Yang and five convergences; it is needled in order to activate spirit and resuscitate the brain in traditional Chinese medicine. Therefore, the purpose of the present study is to investigate the effect of acupuncture stimulation at the Baihui acupoint on cerebral infarct and dopamine levels. A chronic cerebral hypoperfusion animal model was established by permanent ligation of both common carotid arteries; a cerebral infarct animal model was established by blocking the blood flow of both common carotid arteries and the right middle cerebral artery for 90 min followed by reperfusion in Sprague-Dawly (SD) rats. The Baihui acupoint was stimulated for 20 min 3 days per week for 4 weeks. The cognitive and memory functions were evaluated by measuring the successful rates for rats to negotiate an 8-arm radial maze test; the test was performed after operation once a week for 4 weeks. Finally, the rats were sacrificed and their brains were removed; the dopamine levels in brain tissue were measured and the percentage of right to left hemisphere area was calculated. The results indicated that acupuncture stimulation (AS) did not increase the success rate of performing the 8-arm radial maze in chronic cerebral hypoperfusion and cerebral ischemia-reperfusion injured rat models. AS increased dopamine levels in the right cerebral cortex and hippocampus in the chronic cerebral hypoperfusion rats, and increased dopamine levels of the cerebral cortex in the cerebral ischemia-reperfusion injured rat's models. The neurological deficit score was similar between control and AS groups 24 hours after reperfusion, whereas the AS group comprised of ischemia-reperfusion injured rats had a greater percentage of right to left hemisphere area than the control group. In conclusion, AS at the Baihui acupoint for 4 weeks increased dopamine levels in the brain tissue of chronic cerebral hypoperfusion rats and of cerebral ischemia-reperfusion injured rats. The AS also reduced brain atrophy after cerebral infarct, suggesting that AS at the Baihui acupoint acts as neuroprotector. However, regular stimulation at the Baihui acupoint enhances cognition and memory functions need further study.

Acupuntura , Infarto Cerebral/prevenção & controle , Dopamina/metabolismo , Traumatismo por Reperfusão/prevenção & controle , Animais , Infarto Cerebral/metabolismo , Infarto Cerebral/fisiopatologia , Doença Crônica , Masculino , Aprendizagem em Labirinto , Ratos , Ratos Sprague-Dawley , Traumatismo por Reperfusão/metabolismo
Am J Chin Med ; 33(4): 599-611, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-16173534


Our previous studies showed that Gastrodia elata (GE), an herb used in traditional Chinese medicine, has both anti-convulsive and free radical-scavenging activities in kainic acid (KA)-treated rats. The aim of the present study was to further investigate possible physiological mechanisms of GE against activities of neuronal nitric oxide synthase (nNOS) and microglia in KA-treated rats; 0.5 g/kg and 1.0 g/kg of GE extract were administered orally, whereas 20 mg/kg of N-nitro-L-arginine methyl ester (L-NAME) was administered intraperitoneally (ip), both at 30 minutes prior to KA (2 microg/2 microl) being injected into the right hippocampus region of rats. ED1-staining, apoptotic, inducible nitric oxide synthase (iNOS), and nNOS-staining cells were observed in the hippocampus region. The results indicated that 1.0 g/kg of GE and 20 mg/kg of L-NAME reduced the counts of ED1-stained cells, and 0.5 g/kg and 1.0 g/kg of GE, and 20 mg/kg of L-NAME reduced the numbers of apoptotic cells and nNOS-staining cells. In addition, 20 mg/kg of L-NAME also reduced the numbers of iNOS-staining cells, but 0.5 g/kg and 1.0 g/kg of GE did not. This study demonstrated that GE was able to reduce nNOS, microglia activation and apoptosis, suggesting that GE has a protective effect against neuronal damage in KA-treated rats.

Encefalopatias/tratamento farmacológico , Medicamentos de Ervas Chinesas/farmacologia , Gastrodia , Microglia/efeitos dos fármacos , Proteínas do Tecido Nervoso/antagonistas & inibidores , Fármacos Neuroprotetores/farmacologia , Óxido Nítrico Sintase/antagonistas & inibidores , Animais , Apoptose/efeitos dos fármacos , Encefalopatias/induzido quimicamente , Encefalopatias/patologia , Agonistas de Aminoácidos Excitatórios , Hipocampo/enzimologia , Hipocampo/patologia , Ácido Caínico , Masculino , Microglia/patologia , Proteínas do Tecido Nervoso/metabolismo , Óxido Nítrico Sintase/metabolismo , Óxido Nítrico Sintase Tipo I , Óxido Nítrico Sintase Tipo II , Ratos , Ratos Sprague-Dawley