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홈 > 간행물 권호
  • 발행기관: 대한생리학회-대한약리학회
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The Korean Journal of Physiology & Pharmacology

  • 발행기관 : 대한생리학회-대한약리학회(The Korean Journal of Physiology & Pharmacology Editorial Office)
  • 출처구분 : 학회
  • 간행물유형 : 학술저널
  • 발행주기 : 격월간 (발행월:1,3,5,7,9,11)
  • Print ISSN : 1226-4512
  • Online ISSN : 2093-3827
  • 등재정보 : KCI 등재
The Korean Journal of Physiology & Pharmacology
검색결과 =
11
Protective effects and mechanism of coenzyme Q10 and vitamin C on doxorubicin-induced gastric mucosal injury and effects of intestinal flora
Protective effects and mechanism of coenzyme Q10 and vitamin C on doxorubicin-induced gastric mucosal injury and effects of intestinal flora
Xiaomeng Zhao;Xueke Feng;Nan Ye;Panpan Wei;Zhanwei Zhang;Wenyu Lu
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 261-272 (12 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
Doxorubicin (Dox) is widely used to the treatment of cancer, however, it could cause damage to gastric mucosa. To investigate the protective effects and related mechanisms of coenzyme Q10 (CoQ10) and vitamin C (VC) on Dox-induced gastric mucosal injury, we presented the survey of the 4 groups of the rats with dif-ferent conditions. The results showed Dox treatment significantly induced GES-1 apoptosis, but preconditioning in GES-1 cells with VC or CoQ10 significantly inhib-ited the Dox-induced decrease and other harm effects, including the expression and of IκKβ, IκBα, NF-κB/p65 and tumor necrosis factor (TNF-α) in GES-1 cells. Moreover, high-throughput sequencing results showed Dox treatment increased the number of harmful gut microbes, and CoQ10 and VC treatment inhibited this effect. CoQ10 and VC treatment inhibits Dox-induced gastric mucosal injury by inhibiting the activation of the IkKB/IκBα/NF-κB/p65/TNF-α pathway, promoting anti-inflammatory effects of gastric tissue and regulating the composition of the intestinal flora.
Vanillin oxime inhibits lung cancer cell proliferation and activates apoptosis through JNK/ERK-CHOP pathway
Vanillin oxime inhibits lung cancer cell proliferation and activates apoptosis through JNK/ERK-CHOP pathway
Jie Shen;Zhixiang Su
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 273-280 (8 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
Lung cancer despite advancement in the medical field continues to be a major threat to human lives and accounts for a high proportion of fatalities caused by cancers globally. The current study investigated vanillin oxime, a derivative of vanillin, against lung cancer cells for development of treatment and explored the mechanism. Cell viability changes by vanillin oxime were measured using MTT as-say. Vanillin oxime-mediated apoptosis was detected in A549 and NCI-H2170 cells at 48 h of exposure by flow cytometry. The CEBP homologous protein (CHOP) and death receptor 5 (DR5) levels were analysed by RT-PCR and protein levels by West-ern blotting. Vanillin oxime in concentration-dependent way suppressed A549 and NCI-H2170 cell viabilities. On exposure to 12.5 and 15 μM concentrations of vanillin oxime elevated Bax, caspase-3, and -9 levels in A549 and NCI-H2170 cells were ob-served. Vanillin oxime exposure suppressed levels of Bcl-2, survivin, Bcl-xL, cFLIP, and IAPs proteins in A549 and NCI-H2170 cells. It stimulated significant elevation in DR4 and DR5 levels in A549 and NCI-H2170 cells. In A549 and NCI-H2170 cells vanillin ox-ime exposure caused significant (p < 0.05) enhancement in CHOP and DR5 mRNA ex-pression. Vanillin oxime exposure of A549 and NCI-H2170 cells led to significant (p < 0.05) enhancement in levels of phosphorylated extracellular-signal-regulated kinase and c-Jun N-terminal kinase. Thus, vanillin oxime inhibits pulmonary cell proliferation via induction of apoptosis through tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mediated pathway. Therefore, vanillin oxime may be studied further to develop a treatment for lung cancer.
Whole body hypoxic preconditioning-mediated multiorgan protection in db/db mice via nitric oxide-BDNF-GSK-3β-Nrf2 signaling pathway
Whole body hypoxic preconditioning-mediated multiorgan protection in db/db mice via nitric oxide-BDNF-GSK-3β-Nrf2 signaling pathway
Yuefang Li;Yan Huang;Xi Cheng;Youjun He;Xin Hu
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 281-296 (16 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
The beneficial effects of hypoxic preconditioning are abolished in the diabetes. The present study was designed to investigate the protective effects and mechanisms of repeated episodes of whole body hypoxic preconditioning (WBHP) in db/db mice. The protective effects of preconditioning were explored on diabetes-induced vascular dysfunction, cognitive impairment and ischemia-reperfusion (IR)-induced increase in myocardial injury. Sixteen-week old db/db (diabetic) and C57BL/6 (non-diabetic) mice were employed. There was a significant impairment in cognitive function (Morris Water Maze test), endothelial function (acetylcholine-induced relaxation in aortic rings) and a significant increase in IR-induced heart in-jury (Langendorff apparatus) in db/db mice. WBHP stimulus was given by exposing mice to four alternate cycles of low (8%) and normal air O2 for 10 min each. A single episode of WBHP failed to produce protection; however, two and three episodes of WBHP significantly produced beneficial effects on the heart, brain and blood vessels. There was a significant increase in the levels of brain-derived neurotrophic factor (BDNF) and nitric oxide (NO) in response to 3 episodes of WBHP. Moreover, pretreat-ment with the BDNF receptor, TrkB antagonist (ANA-12) and NO synthase inhibitor (L-NAME) attenuated the protective effects imparted by three episodes of WBHP. These pharmacological agents abolished WBHP-induced restoration of p-GSK-3β/GSK-3βratio and Nrf2 levels in IR-subjected hearts. It is concluded that repeated episodes of WHBP attenuate cognitive impairment, vascular dysfunction and enhancement in IR-induced myocardial injury in diabetic mice be due to increase in NO and BDNF levels that may eventually activate GSK-3β and Nrf2 signaling pathway to confer protec-tion.
Luteolin inhibits H2O2-induced cellular senescence via modulation of SIRT1 and p53
Luteolin inhibits H2O2-induced cellular senescence via modulation of SIRT1 and p53
Ri Zhe Zhu Bing Si Li Shang Shang Gao Jae Ho Seo Byung-Min Choi
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 297-305 (9 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
Luteolin, a sort of flavonoid, has been reported to be involved in neu-roprotective function via suppression of neuroinflammation. In this study, we in-vestigated the protective effect of luteolin against oxidative stress-induced cellular senescence and its molecular mechanism using hydrogen peroxide (H2O2)-induced cellular senescence model in House Ear Institute-Organ of Corti 1 cells (HEI-OC1). Our results showed that luteolin attenuated senescent phenotypes including alterations of morphology, cell proliferation, senescence-associated β-galactosidase expression, DNA damage, as well as related molecules expression such as p53 and p21 in the oxidant challenged model. Interestingly, we found that luteolin induces expression of sirtuin 1 in dose- and time-dependent manners and it has protective role against H2O2-induced cellular senescence by upregulation of sirtuin 1 (SIRT1). In contrast, the inhibitory effect of luteolin on cellular senescence under oxidative stress was abolished by silencing of SIRT1. This study indicates that luteolin effectively protects against oxidative stress-induced cellular senescence through p53 and SIRT1. These results suggest that luteolin possesses therapeutic potentials against age-related hearing loss that are induced by oxidative stress.
Wnt-C59 inhibits proinflammatory cytokine expression by reducing the interaction between -catenin and NF-κB in LPS-stimulated epithelial and macrophage cells
Wnt-C59 inhibits proinflammatory cytokine expression by reducing the interaction between -catenin and NF-κB in LPS-stimulated epithelial and macrophage cells
Jaewoong Jang;Jaewon Song;Inae Sim;Yoosik Yoon
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 307-319 (13 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
Dysregulation of the Wnt pathway causes various diseases including cancer, Parkinson’s disease, Alzheimer’s disease, schizophrenia, osteoporosis, obesity and chronic kidney diseases. The modulation of dysregulated Wnt pathway is abso-lutely necessary. In the present study, we evaluated the anti-inflammatory effect and the mechanism of action of Wnt-C59, a Wnt signaling inhibitor, in lipopolysaccharide (LPS)-stimulated epithelial cells and macrophage cells. Wnt-C59 showed a dose-de-pendent anti-inflammatory effect by suppressing the expression of proinflammatory cytokines including IL6, CCL2, IL1A, IL1B, and TNF in LPS-stimulated cells. The dysreg-ulation of the Wnt/β-catenin pathway in LPS stimulated cells was suppressed by Wnt-C59 treatment. The level of β-catenin, the executor protein of Wnt/β-catenin path-way, was elevated by LPS and suppressed by Wnt-C59. Overexpression of β-catenin rescued the suppressive effect of Wnt-C59 on proinflammatory cytokine expression and nuclear factor-kappa B (NF-κB) activity. We found that the interaction between β-catenin and NF-κB, measured by co-immunoprecipitation assay, was elevated by LPS and suppressed by Wnt-C59 treatment. Both NF-κB activity for its target DNA binding and the reporter activity of NF-κB-responsive promoter showed identical patterns with the interaction between β-catenin and NF-κB. Altogether, our findings suggest that the anti-inflammatory effect of Wnt-C59 is mediated by the reduction of the cellular level of β-catenin and the interaction between β-catenin and NF-κB, which results in the suppressions of the NF-κB activity and proinflammatory cytokine expression.
Protective effects of lutein against vancomycin-induced acute renal injury in mice via upregulation of peroxisome proliferator-activated receptor gamma/nuclear factor erythroid 2-related factor 2 and inhibition nuclear factor-kappaB/caspase 3
Protective effects of lutein against vancomycin-induced acute renal injury in mice via upregulation of peroxisome proliferator-activated receptor gamma/nuclear factor erythroid 2-related factor 2 and inhibition nuclear factor-kappaB/caspase 3
Promise M. Emeka;Sahibzada T. Rasool;Mohamed A. Morsy;Mohamed I. Hairul Islam;Muhammad S. Chohan
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 321-331 (11 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
Vancomycin, an antibiotic used occasionally as a last line of treatment for methicillin-resistant Staphylococcus aureus, is reportedly associated with nephro-toxicity. This study aimed at evaluating the protective effects of lutein against vanco-mycin-induced acute renal injury. Peroxisome proliferator-activated receptor gamma (PPARγ) and its associated role in renoprotection by lutein was also examined. Male BALB/c mice were divided into six treatment groups: control with normal saline, lu-tein (200 mg/kg), vancomycin (250 mg/kg), vancomycin (500 mg/kg), vancomycin (250 mg/kg) with lutein, and vancomycin (500 mg/kg) with lutein groups; they were euthanized after 7 days of treatment. Thereafter, samples of blood, urine, and kidney tissue of the mice were analyzed, followed by the determination of levels of N-acetyl-β-D-glucosaminidase (NAG) in the urine, renal creatine kinase; protein carbonyl, malondialdehyde, and caspase-3 in the kidney; and the expression of PPARγ, nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-kappaB (NF-κB) in renal tissue. Results showed that the levels of protein carbonyl and malondialdehyde, and the activity of NAG, creatine kinase and caspase-3, were significantly increased in the vancomycin-treatment groups. Moreover, the levels of Nrf2 significantly decreased, while NF-κB expression increased. Lutein ameliorated these effects, and significantly increased PPARγ expression. Furthermore, it attenuated vancomycin-induced histo-logical alterations such as, tissue necrosis and hypertrophy. Therefore, we conclude that lutein protects against vancomycin-induced renal injury by potentially upregu-lating PPARγ/Nrf2 expression in the renal tissues, and consequently downregulating the pathways: inflammation by NF-κB and apoptosis by caspase-3
The beneficial effect of glycerophosphocholine to local fat accumulation: a comparative study with phosphatidylcholine and aminophylline
The beneficial effect of glycerophosphocholine to local fat accumulation: a comparative study with phosphatidylcholine and aminophylline
Go Woon KimpSung Hyun Chung
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 333-339 (7 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
Injection lipolysis or mesotherapy gained popularity for local fat dissolve as an alternative to surgical liposuction. Phosphatidylcholine (PPC) and aminophyl-line (AMPL) are commonly used compounds for mesotherapy, but their efficacy and safety as lipolytic agents have been controversial. Glycerophosphocholine (GPC) is a choline precursor structurally similar to PPC, and thus introduced in aesthetics as an alternative for PPC. This study aimed to evaluate the effects of GPC on adipocytes dif-ferentiation and lipolysis and compared those effects with PPC and AMPL using in vi-tro and in vivo models. Adipogenesis in 3T3-L1 was measured by Oil Red O staining. Lipolysis was assessed by measuring the amount of glycerol released in the culture media. To evaluate the lipolytic activity of GPC on a physiological condition, GPC was subcutaneously injected to one side of inguinal fat pads for 3 days. Lipolytic activity of GPC was assessed by hematoxylin and eosin staining in adipose tissue. GPC signifi-cantly suppressed adipocyte differentiation of 3T3-L1 in a concentration-dependent manner (22.3% inhibition at 4 mM of GPC compared to control). Moreover, when lipolysis was assessed by glycerol release in 3T3-L1 adipocytes, 6 mM of GPC stimu-lated glycerol release by two-fold over control. Subcutaneous injection of GPC into the inguinal fat pad of mice significantly reduced the mass of fat pad and the size of adipocytes of injected site, and these effects of GPC were more prominent over PPC and AMPL. Taken together, these results suggest that GPC is the potential therapeu-tic agent as a local fat reducer.
Cardamonin exerts a protective effect against autophagy and apoptosis in the testicles of diabetic male rats through the expression of Nrf2 via p62-mediated Keap-1 degradation
Cardamonin exerts a protective effect against autophagy and apoptosis in the testicles of diabetic male rats through the expression of Nrf2 via p62-mediated Keap-1 degradation
Shereen M. Samir;Mahmoud Elalfy;Eman Mohamad El Nashar;Mansour A. Alghamdi;Eman Hamza;Mohamed Saad Serria;Mona G. Elhadidy
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 341-354 (14 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
Cardamonin (CARD) is a chalconoid with anti-inflammatory and anti-oxidant properties, and it is present in several plants. We sought to explore whether CARD exerts any positive effects against hyperglycemia-induced testicular dysfunc-tion caused by type 2 diabetes and aimed to identify its possible intracellular path-ways. Adult male rats were subdivided into six groups: control, CARD, diabetic (DM), DM + glibenclamide (GLIB), DM + CARD and DM + GLIB + CARD. Type 2 DM induced a significant increase in blood glucose and insulin resistance, along with diminished serum insulin, testosterone and gonadotropins levels, which were associated with the impairment of key testicular androgenic enzymes and cellular redox balance. Administration of CARD at a dose of 80 mg/kg for 4 weeks effectively normalized all of these alterations, and the improvement was confirmed by epididymal sperm analysis. After treatment with CARD, the pathological changes in spermatogenic tubules were markedly improved. Significantly, CARD upregulated testicular glucose transporter-8 (GLUT-8) expression and had inhibitory effects on elevated autophagy markers and caspase-3 immunoreactive cells. Furthermore, our results revealed that CARD was able to attenuate damage via activation of Nrf2 through the p62-dependent degradation of testicular anti-Kelch-like ECH-associated protein-1 (Keap-1). In conclusion, this study suggests that CARD provides protection against diabetic stress-mediated testicular damage. The use of CARD with conventional anti-diabetic therapy was associated with improved efficacy compared with conventional therapy alone.
Deletion of adipose triglyceride lipase abolishes blood flow increase after β3-adrenergic stimulation in visceral adipose tissue of mice
Deletion of adipose triglyceride lipase abolishes blood flow increase after β3-adrenergic stimulation in visceral adipose tissue of mice
Hye-Jin Lee;Bo-Yeong Jin;Mi-Rae Park;Kwan Sik Seo;Yong Taek Jeong;Sang-Hyun Choi;Dong-Hoon Kim
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 355-363 (9 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
Dynamic changes in adipose tissue blood flow (ATBF) with nutritional sta-tus play a role in the regulation of metabolic and endocrine functions. Activation of the sympathetic nervous system via β-adrenergic receptors (β-AR) contributes to the control of postprandial enhancement of ATBF. Herein, we sought to identify the role of each β-AR subtype in the regulation of ATBF in mice. We monitored the changes in visceral epididymal ATBF (VAT BF), induced by local infusion of dobutamine, salbu-tamol, and CL316,243 (a selective β1-, β2-, and β3-AR agonist, respectively) into VAT of lean CD-1 mice and global adipose triglyceride lipase (ATGL) knockout (KO) mice, using laser Doppler flowmetry. Administration of CL316,243, known to promote li-polysis in adipocytes, significantly increased VAT BF of CD-1 mice to a greater extent compared to that of the vehicle, whereas administration of dobutamine or salbuta-mol did not produce significant differences in VAT BF. The increase in VAT BF induced by β3-AR stimulation disappeared in ATGL KO mice as opposed to their wild-type (WT) littermates, implying a role of ATGL-mediated lipolysis in the regulation of VAT BF. Different vascular reactivities occurred despite no significant differences in vessel density and adiposity between the groups. Additionally, the expression levels of the angiogenesis-related genes were significantly higher in VAT of ATGL KO mice than in that of WT, implicating an association of ATBF responsiveness with angiogenic activ-ity in VAT. Our findings suggest a potential role of β3-AR signaling in the regulation of VAT BF via ATGL-mediated lipolysis in mice.
Rapamycin reduces orofacial nociceptive responses and microglial p38 mitogen-activated protein kinase phosphorylation in trigeminal nucleus caudalis in mouse orofacial formalin model
Rapamycin reduces orofacial nociceptive responses and microglial p38 mitogen-activated protein kinase phosphorylation in trigeminal nucleus caudalis in mouse orofacial formalin model
Ji-Hee Yeo;Sol-Ji Kim;Dae-Hyun Roh
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 365-374 (10 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
The mammalian target of rapamycin (mTOR) plays a role in various cellu-lar phenomena, including autophagy, cell proliferation, and differentiation. Although recent studies have reported its involvement in nociceptive responses in several pain models, whether mTOR is involved in orofacial pain processing is currently unex-plored. This study determined whether rapamycin, an mTOR inhibitor, reduces noci-ceptive responses and the number of Fos-immunoreactive (Fos-ir) cells in the trigem-inal nucleus caudalis (TNC) in a mouse orofacial formalin model. We also examined whether the glial cell expression and phosphorylated p38 (p-p38) mitogen-activated protein kinases (MAPKs) in the TNC are affected by rapamycin. Mice were intraperi-toneally given rapamycin (0.1, 0.3, or 1.0 mg/kg); then, 30 min after, 5% formalin (10 μl) was subcutaneously injected into the right upper lip. The rubbing responses with the ipsilateral forepaw or hindpaw were counted for 45 min. High-dose rapamycin (1.0 mg/kg) produced significant antinociceptive effects in both the first and second phases of formalin test. The number of Fos-ir cells in the ipsilateral TNC was also reduced by high-dose rapamycin compared with vehicle-treated animals. Further-more, the number of p-p38-ir cells the in ipsilateral TNC was significantly decreased in animals treated with high-dose rapamycin; p-p38 expression was co-localized in microglia, but not neurons and astrocytes. Therefore, the mTOR inhibitor, rapamycin, reduces orofacial nociception and Fos expression in the TNC, and its antinociceptive action on orofacial pain may be associated with the inhibition of p-p38 MAPK in the microglia.
Sepsis induces variation of intestinal barrier function in different phase through nuclear factor kappa B signaling
Sepsis induces variation of intestinal barrier function in different phase through nuclear factor kappa B signaling
Ying-Ya Cao;Zhong-Han Wang;Qian-Cheng Xu;Qun Chen;Zhen Wang;Wei-Hua Lu
대한생리학회-대한약리학회 / The Korean Journal of Physiology & Pharmacology 제25권 제4호 / 2021 / 375-383 (9 pages)
의약학>의학일반 / KDC : 기술과학 > 의학 / KCI : 의약학 > 약리학
초록보기
The intestinal barrier function disrupted in sepsis, while little is known about the variation in different phases of sepsis. In this study, mouse models of sepsis were established by caecal ligation and puncture (CLP). The H&E staining of sections and serum diamine oxidase concentration were evaluated at different timepoint af-ter CLP. TUNEL assay and EdU staining were performed to evaluate the apoptosis and proliferation of intestinal epithelium. Relative protein expression was assessed by Western blotting and serum concentrations of pro-inflammatory cytokines was mea-sured by ELISA. The disruption of intestinal barrier worsened in the first 24 h after the onset of sepsis and gradually recovered over the next 24 h. The percentage of apop-totic cell increased in the first 24 h and dropped at 48 h, accompanied with the prolif-erative rate of intestinal epithelium inhibited in the first 6 h and regained in the later period. Furthermore, the activity of nuclear factor kappa B (NF-κB) presented similar trend with the intestinal barrier function, shared positive correction with apoptosis of intestinal epithelium. These findings reveal the conversion process of intestinal barrier function in sepsis and this process is closely correlated with the activity of NF-κB signaling.