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   2021| March-April  | Volume 64 | Issue 2  
    Online since April 28, 2021

 
 
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ORIGINAL ARTICLES
Tau phosphorylation and cochlear apoptosis cause hearing loss in 3×Tg-AD Mouse Model of Alzheimer's Disease
Sheue-Er Wang, Chung-Hsin Wu
March-April 2021, 64(2):61-71
DOI:10.4103/CJP.CJP_79_20  PMID:33938816
Clinically typical dementia Alzheimer's disease (AD) is associated with abnormal auditory processing. However, possible molecular mechanisms responsible for the auditory pathology of AD patients are not known. According to our past research findings that the thresholds of auditory brainstem response, but not distortion product otoacoustic emissions, were significantly increased in AD mice from 9 months of age and thereafter. Thus, we further explored the possible mechanism of auditory degradation of 3×Tg-AD mice in this study. Our histochemical staining evidence showed the cochlear spiral ganglion neurons (SGN), but not the cochlear hair cells, were lost significantly in the cochlea of 3×Tg-AD mice from 9 months of age and thereafter. Our immunostaining and western blotting evidence showed that phosphorylated tau protein (p-Tau), p-glycogen synthase kinase 3, neurofilament, and apoptosis-related p53, Bcl2-associated X protein, cytochrome c, caspase-9, and caspase-3 were gradually increased, but B-cell lymphoma 2 was gradually decreased with age growth in the cochlea of 3×Tg-AD mice. We suggested that tau hyperphosphorylation and p-Tau 181 aggregation, and mitochondria- and endoplasmic reticulum stress-mediated apoptosis may play a role in the degeneration of SGN in the cochlea. Progressive SGN degeneration in the cochlea may contribute to hearing loss of aging 3×Tg-AD mice.
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Characterization of Ca2+-Sensing Receptor-Mediated Ca2+ Influx in Microvascular bEND.3 Endothelial Cells
Iat-Lon Leong, Tien-Yao Tsai, Lian-Ru Shiao, Yu-Mei Zhang, Kar-Lok Wong, Paul Chan, Yuk-Man Leung
March-April 2021, 64(2):80-87
DOI:10.4103/cjp.cjp_93_20  PMID:33938818
Ca2+-sensing receptors (CaSR), activated by elevated concentrations of extracellular Ca2+, have been known to regulate functions of thyroid cells, neurons, and endothelial cells (EC). In this report, we studied CaSR-mediated Ca2+ influx in mouse cerebral microvascular EC (bEND.3 cells). Cytosolic free Ca2+ concentration and Mn2+ influx were measured by fura-2 microfluorometry. High (3 mM) Ca2+ (CaSR agonist), 3 mM spermine (CaSR agonist), and 10 μM cinacalcet (positive allosteric modulator of CaSR) all triggered Ca2+ influx; however, spermine, unlike high Ca2+ and cinacalcet, did not promote Mn2+ influx and its response was poorly sensitive to SKF 96365, a TRP channel blocker. Consistently, 2-aminoethoxydiphenyl borate and ruthenium red (two other general TRP channel blockers) suppressed Ca2+ influx triggered by cinacalcet and high Ca2+ but not by spermine. Ca2+ influx triggered by high Ca2+, spermine, and cinacalcet was similarly suppressed by A784168, a potent and selective TRPV1 antagonist. Our results suggest that CaSR activation triggered Ca2+ influx via TRPV1 channels; intriguingly, pharmacological, and permeability properties of such Ca2+ influx depended on the stimulating ligands.
  1,841 249 -
Effects of moderate intensity endurance training and high-intensity interval training on the reproductive parameters of wistar rats overfed in infancy
Mariana Bolotari, Ana Eliza Andreazzi, Carlos Gabriel de Lade, Vinicius Moreira Goncalves Costa, Martha de Oliveira Guerra, Vera Maria Peters
March-April 2021, 64(2):106-114
DOI:10.4103/cjp.cjp_96_20  PMID:33938821
Studies indicate that rapid weight gain at critical development stages, such as the lactation period, is associated with the development of obesity, cardiovascular diseases, and diabetes in the long term. In addition to metabolic changes during adulthood, overweight/obesity may influence reproductive function. Human and animal studies suggest that lifestyle changes through exercise and/or controlled diet result in improved semen quality in obese individuals. However, the relationship between exercise volume/intensity and reproductive capacity effects remains inconclusive. The present study aimed to evaluate the effects of moderate intensity endurance training and high-intensity interval training (HIIT) on the reproductive parameters of lactating overfed male Wistar rats. Postnatal overfeeding was induced by applying the litter size reduction method. Forty males Wistar rats were used, divided into four groups: one with control litters (CLs) (10 animals/litter-sedentary) and three with small litters (SLs) (4 animals/litter), divided into sedentary, moderate endurance training, and HIIT. Morphologic, metabolic, and reproductive variables were analyzed. SL sedentary group showed increased body weight, adiposity, and decreased relative weight of the seminal vesicle, prostate, and epididymis as well as changes in the insulin tolerance and oral glucose tolerance tests glycemic tests compared to CL sedentary group. Endurance and HIIT protocols were efficient in improving the glycemic metabolism, central fat accumulation of trained groups and did not affect reproductive parameters. Endurance and HIIT protocols proved to be effective in reversing these metabolic changes without impairing the evaluated reproductive parameters.
  1,655 285 -
Protection of the neurovascular unit from calcium-related ischemic injury by linalyl acetate
Yu Shan Hsieh, You Kyoung Shin, Geun Hee Seol
March-April 2021, 64(2):88-96
DOI:10.4103/cjp.cjp_94_20  PMID:33938819
Calcium-related ischemic injury (CRII) can damage cells of the neurovascular unit (NVU). Here, we investigate the protective effects of linalyl acetate (LA) against CRII-induced NVU damage and evaluate the underlying mechanisms. The protective effects of LA in cell lines representative of NVU components (BEND, SH-SY5Y, BV2, and U373 cells) were evaluated following exposure to oxygen-glucose deprivation/reoxygenation alone (OGD/R-only) or OGD/R in the presence of 5 mM extracellular calcium ([Ca2+]o) to mimic CRII. LA reversed damage under OGD/R-only conditions by blocking p47phox/NADPH oxidase (NOX) 2 expression, reactive oxygen species (ROS) production, nitric oxide (NO) abnormality, and lactate dehydrogenase (LDH) release only in the BEND cells. However, under CRII-mimicking conditions, LA reversed NO abnormality and matrix metalloproteinase (MMP)-9 activation in the BEND murine brain endothelial cells; inhibited p47phox expression in the human SH-SY5Y neural-like cells; decreased NOX2 expression and ROS generation in the BV2 murine microglial cells; and reduced p47phox expression in the U373 human astrocyte-like cells. Importantly, LA protected against impairment of the neural cells, astrocytes, and microglia, all of which are cellular components of the NVU induced by exposure to CRII-mimicking conditions, by reducing LDH release. We found that LA exerted a protective effect in the BEND cells that may differ from its protective effects in other NVU cell types, following OGD/R-induced damage in the context of elevated [Ca2+]o.
  1,638 241 -
Deficit of female sex hormones desensitizes rat cardiac mitophagy
Theerachat Kampaengsri, Marisa Ponpuak, Jonggonnee Wattanapermpool, Tepmanas Bupha-Intr
March-April 2021, 64(2):72-79
DOI:10.4103/cjp.cjp_102_20  PMID:33938817
Long-term deprivation of female sex hormones has been shown to mediate accumulation of damaged mitochondria in ventricular muscle leading to cardiovascular dysfunction. Therefore, the roles of female sex hormones in mitochondrial quality control are closely focused. In the present study, depletion of female sex hormones impairing mitochondrial autophagy in the heart was hypothesized. Cardiac mitophagy was therefore investigated in the heart of 10-week ovariectomized (OVX) and sham-operated (SHAM) rats. By using isolated mitochondria preparation, results demonstrated an increase in mitochondrial PTEN-induced kinase 1 accumulation in the sample of OVX rats indicating mitochondrial outer membrane dysfunction. However, no change in p62 and LC3-II translocation to mitochondria was observed between two groups indicating unresponsiveness of mitophagosome formation in the OVX rat heart. This loss might be resulted from significant decreases in Parkin and Bcl2l13 expression, but not Bnip3 activation. In summary, results suggest that mitochondrial abnormality in the heart after deprivation of female sex hormones could consequently be due to desensitization of mitophagy process.
  1,459 288 -
Study on the time-effectiveness of exercise preconditioning on heart protection in exhausted rats
Ye Su, Yang Wang, Peng Xu, Yawei Sun, Zheng Ping, Heling Huang, Xuebin Cao
March-April 2021, 64(2):97-105
DOI:10.4103/CJP.CJP_65_20  PMID:33938820
To investigate the persistence time and the effectiveness of exercise preconditioning (EP) on myocardial protection in exhausted rats from myocardial enzymes, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function after cessation of exercise training. One hundred and twelve healthy male Sprague–Dawley rats were randomly divided into seven groups (n = 16): control group (CON), exhaustive exercise (EE) group, EP group, and EE after EP (EP + EE); furthermore, EP + EE group was randomly divided into 1D, 3D, 9D, and 18D groups (1D, 3D, 9D, and 18D) and performed exhaustive treadmill exercise at a speed of 30 m/min on the 1st, 3rd, 9th, and 18th days separately after EP exercise stopped. We detected the serum contents of N-terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) by the enzyme-linked immunosorbent assays method, recorded ECG, detected heart function by pressure volume catheter, measured the respiratory rates of rat myocardial mitochondria state 3 and 4 of complex I, complex II, and IV by high-resolution breathing apparatus. EP could decrease the serum content of NT-proBNP and cTnI, improved the electrical derangement and the left ventricular function in exhausted rats. Moreover, the protective effect was more obvious in the 9th day after EP stopped, whereas it would disappear when EP stopped for more than 18 days. Compared with EE group, the respiratory rate value of myocardial mitochondrial complex increased in 1D, 3D, and 9D groups. Therefore, the protective effect of EP on the heart of exhausted rats decreased with the prolongation of stopping training time, and the effect was significant within 3 days of discontinuing training, then decreased gradually, and completely disappeared in the 18th day. EP enhanced the cardiac function in exhausted rats through raising the nicotinamide adenine diphosphate hydride (NADH) electron transport chain and increased the respiration rates of mitochondrial respiratory complex I and IV state 3, thereby improved myocardial mitochondrial respiratory function and energy metabolism.
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