排序方式: 共有91条查询结果,搜索用时 703 毫秒
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Siripong Palee Wanitchaya Minta Duangkamol Mantor Wissuta Sutham Sasiwan Kerdphoo Wasana Pratchayasakul Siriporn C. Chattipakorn Nipon Chattipakorn 《Journal of cellular physiology》2019,234(5):6983-6991
The incidence of cardiovascular disease and metabolic syndrome increases after the onset of menopause, giving evidence for the vital role of estrogen. Intracellular calcium [Ca2+]i regulation plays an important role in the maintenance of left ventricular (LV) contractile function. Although either estrogen deprivation or obesity has been shown to strongly affect the metabolic status and LV function, the effects of estrogen deprivation on the cardiometabolic status and cardiac [Ca 2+]i regulation in the obese-insulin resistant condition have never been investigated. Our hypothesis was that estrogen deprivation aggravates LV dysfunction through the increased impairment of [Ca 2+]i homeostasis in obese-insulin resistant rats. Female rats were fed on either a high-fat (HFD, 59.28% fat) or normal (ND, 19.77% fat) diet for 13 weeks. Then, rats were divided into sham (HFS and NDS) operated or ovariectomized (HFO and NDO) groups. Six weeks after surgery, metabolic status, LV function and incidence of [Ca 2+]i transients were determined. NDO, HFS, and HFO rats had evidence of obese-insulin resistance indicated by increased body weight with hyperinsulinemia and euglycemia. Although NDO, HFS, and HFO rats had markedly reduced %LV fractional shortening, E/A ratio and decreased [Ca 2+]i transient amplitude and decay rate, HFO rats had the most severe impairments. These findings indicate that estrogen deprivation had a strong impact on abnormal LV function through [Ca 2+]i regulation. In addition, evidence was found that in obese-insulin resistant rats, estrogen deprivation severely aggravates LV dysfunction via increased impairment of [Ca 2+]i homeostasis. 相似文献
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Phoom Narongkiatikhun Siriporn C. Chattipakorn Nipon Chattipakorn 《Journal of cellular and molecular medicine》2022,26(2):249
Diabetic kidney disease (DKD) is a common microvascular complication among diabetic patients. Once the DKD has developed, most of the patients inevitably progress to the end‐stage renal disease (ESRD). Although many new therapeutic strategies have attempted to demolish the root of the pathogenesis of DKD, the residual risks of ESRD still remained. Alteration of mitochondrial dynamics towards mitochondrial fission concurrent with the mitochondrial dysfunction is the characteristic that is usually seen in various diseases, including DKD. It has been proposed that those perturbation and their cooperative networks could be responsible for the residual risk of ESRD in DKD patients. In this review, the collective evidence of alteration in mitochondrial dynamics and their associations with the mitochondrial function from in vitro, in vivo and clinical reports of DKD are comprehensively summarized and discussed. In addition, both basic and clinical reports regarding the pharmacological interventions that showed an impact on the mitochondrial dynamics, and the correlation with the renal parameters in DKD is presented. Understanding these complex mechanisms in combination with the existing therapeutic modalities could bring a new opportunity to overcome the unresolvable problem of DKD. 相似文献
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Sirikul Thummajitsakul Sirawut Klinbunga Siriporn Sittipraneed 《Biochemical genetics》2010,48(3-4):181-192
A species-diagnostic SCAR marker for identification of the stingless bee (Trigona pagdeni Schwarz) was successfully developed. Initially, amplified fragment length polymorphism analysis was carried out across representatives of 12 stingless bee species using 64 primer combinations. A 284 bp band restrictively found in T. pagdeni was cloned and sequenced. A primer pair (CUTP1-F/R) was designed and tested for species-specificity in 15 stingless bees. The expected 163 bp fragment was successfully amplified in all examined individuals of T. pagdeni (129/129). Nevertheless, cross-species amplification was also observed in T. fimbriata (1/3), T. collina (11/112), T. laeviceps (1/12), and T. fuscobalteata (15/15), but not in other species. SSCP analysis of CUTP1 further differentiated T. fuscobalteata and T. collina from T. pagdeni. Although T. laeviceps, T. fimbriata, and T. pagdeni shared an identical SSCP genotype, they are not taxonomically problematic species. 相似文献
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Kentaro Koide Siriporn Kongsoi Chie Nakajima 《Bioscience, biotechnology, and biochemistry》2013,77(12):2249-2256
ABSTRACTThe inhibitory effect of WQ-3810 on DNA gyrase was assayed to evaluate the potential of WQ-3810 as a candidate drug for the treatment of quinolone resistant Salmonella Typhymurium infection. The inhibitory effect of WQ-3810, ciprofloxacin and nalidixic acid was compared by accessing the drug concentration that halves the enzyme activity (IC50) of purified S. Typhimurium wildtype and mutant DNA gyrase with amino acid substitution at position 83 or/and 87 in subunit A (GyrA) causing quinolone resistance. As a result, WQ-3810 reduced the enzyme activity of both wildtype and mutant DNA gyrase at a lower concentration than ciprofloxacin and nalidixic acid. Remarkably, WQ-3810 showed a higher inhibitory effect on DNA gyrase with amino acid substitutions at position 87 than with that at position 83 in GyrA. This study revealed that WQ-3810 could be an effective therapeutic agent, especially against quinolone resistant Salmonella enterica having amino acid substitution at position 87. 相似文献
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Chanchai Sattayanon Nawee Kungwan Winita Punyodom Puttinan Meepowpan Siriporn Jungsuttiwong 《Journal of molecular modeling》2013,19(12):5377-5385
A theoretical investigation of the ring-opening polymerization (ROP) mechanism of ε-caprolactone (CL) with tin(II) alkoxide, Sn(OR)2 initiators (R?=?n-C4H9, i-C4H9, t-C4H9, n-C6H13, n-C8H17) was studied. The density functional theory at B3LYP level was used to perform the modeled reactions. A coordination-insertion mechanism was found to occur via two transition states. Starting with a coordination of CL onto tin center led to a nucleophilic addition of the carbonyl group of CL, followed by the exchange of alkoxide ligand. The CL ring opening was completed through classical acyl-oxygen bond cleavage. The reaction barrier heights of ε-caprolactone with different initiators were calculated using potential energy profiles. The reaction of ε-caprolactone with Sn(OR)2 having R?=?n-C4H9 has the least value of barrier height compared to other reactions. The rate constants for each reaction were calculated using the transition state theory with TheRATE program. The rate constants are in good agreement with available experimental data. 相似文献
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Jirapas Sripetchwandee Jantira Sanit Nipon Chattipakorn Siriporn C. Chattipakorn 《Life sciences》2013,92(4-5):298-304
AimsAlthough iron overload induces oxidative stress and brain mitochondrial dysfunction, and is associated with neurodegenerative diseases, brain mitochondrial iron uptake has not been investigated. We determined the role of mitochondrial calcium uniporter (MCU) in brain mitochondria as a major route for iron entry. We hypothesized that iron overload causes brain mitochondrial dysfunction, and that the MCU blocker prevents iron entry into mitochondria, thus attenuating mitochondrial dysfunction.Main methodsIsolated brain mitochondria from male Wistar rats were used. Iron (Fe2 + and Fe3 +) at 0–286 μM were applied onto mitochondria at various incubation times (5–30 min), and the mitochondrial function was determined. Effects of MCU blocker (Ru-360) and iron chelator were studied.Key findingsBoth Fe2 + and Fe3 + entered brain mitochondria and caused mitochondrial swelling in a dose- and time-dependent manner, and caused mitochondrial depolarization and increased ROS production. However, Fe2 + caused more severe mitochondrial dysfunction than Fe3 +. Although all drugs attenuated mitochondrial dysfunction caused by iron overload, only an MCU blocker could completely prevent ROS production and mitochondrial depolarization.SignificanceOur findings indicated that iron overload caused brain mitochondrial dysfunction, and that an MCU blocker effectively prevented this impairment, suggesting that MCU could be the major portal for brain mitochondrial iron uptake. 相似文献
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Benjamin Ongnok Thawatchai Khuanjing Titikorn Chunchai Sasiwan Kerdphoo Thidarat Jaiwongkam Nipon Chattipakorn Siriporn C. Chattipakorn 《生物化学与生物物理学报:疾病的分子基础》2021,1867(1):165975
Cardiac ischemia/reperfusion (I/R) injury induces brain pathology. Donepezil, a well-known acetylcholine esterase (AChE) inhibitor, has been proven to exert neuroprotective effects against several neurodegenerative diseases. However, the comprehensive mechanism regarding the therapeutic potential of donepezil on the brain under cardiac I/R injury remains obscure. Here, we hypothesized that treatment with donepezil ameliorates brain pathology following cardiac I/R injury by decreasing blood brain barrier (BBB) breakdown, oxidative stress, neuroinflammation, mitochondrial dysfunction, mitochondrial dynamics imbalance, microglial activation, amyloid-beta (Aβ) accumulation, neuronal apoptosis, and dendritic spine loss. Forty-eight adult male Wistar rats were subjected to surgery for cardiac I/R injury. Then, rats were randomly divided into four groups to receive either (1) saline (vehicle group), donepezil 3 mg/kg via intravenously administered (2) before ischemia (pretreatment group), (3) during ischemia (ischemia group), or (4) at the onset of reperfusion (reperfusion group). At the end of cardiac I/R paradigm, the brains were evaluated for BBB breakdown, brain inflammation, oxidative stress, mitochondrial function, mitochondrial dynamics, microglial morphology, Aβ production, neuronal apoptosis, and dendritic spine density. Administration of donepezil at all time points equally showed an attenuation of brain damage in response to cardiac I/R injury, as indicated by increased expression of BBB junction protein, reduced brain inflammation and oxidative stress, improved mitochondrial function and mitochondrial dynamics, and alleviated Aβ accumulation and microglial activation, resulting in protection of neuronal apoptosis and preservation of dendritic spine number. These findings suggest that donepezil potentially protects brain pathology caused by cardiac I/R injury regardless the timing of treatment. 相似文献