Gap junction blockage promotes cadmium-induced apoptosis in BRL 3A derived from Buffalo rat liver cells

Di Hu,Hui Zou,Tao Han,Junze Xie,Nannan Dai,Liling Zhuo,Jianhong Gu,Jianchun Bian,Yan Yuan,Xuezhong Liu,Zongping Liu 대한수의학회 2016 Journal of Veterinary Science Vol.17 No.1

Gap junctions mediate direct communication between cells; however, toxicological cascade triggered by nonessential metals can abrogate cellular signaling mediated by gap junctions. Although cadmium (Cd) is known to induce apoptosis in organs and tissues, the mechanisms that underlie gap junction activity in Cd-induced apoptosis in BRL 3A rat liver cells has yet to be established. In the present study, we showed that Cd treatment decreased the cell index (a measure of cellular electrical impedance) in BRL 3A cells. Mechanistically, we found that Cd exposure decreased expression of connexin 43 (Cx43), increased expression of p-Cx43 and elevated intracellular free Ca2+ concentration, corresponding to a decrease in gap junctional intercellular communication. Gap junction blockage pretreatment with 18b-glycyrrhizic acid (GA) promoted Cd-induced apoptosis, involving changes in expression of Bax, Bcl-2, caspase-3 and the mitochondrial transmembrane electrical potential (Δym). Additionally, GA was found to enhance ERK and p38 activation during Cd-induced activation of mitogen-activated protein kinases, but had no significant effect on JNK activation. Our results indicated the apoptosis-related proteins and the ERK and p38 signaling pathways may participate in gap junction blockage promoting Cd-induced apoptosis in BRL 3A cells.

Hydrogen sulfide inhibits the growth of Escherichia coli through oxidative damage

Liu-Hui Fu,Zeng-Zheng Wei,Kang-Di Hu,Lan-Ying Hu,Yan-Hong Li,Xiao-Yan Chen,Zhuo Han,Gai-Fang Yao,Hua Zhang 한국미생물학회 2018 The journal of microbiology Vol.56 No.4

Many studies have shown that hydrogen sulfide (H2S) is both detrimental and beneficial to animals and plants, whereas its effect on bacteria is not fully understood. Here, we report that H2S, released by sodium hydrosulfide (NaHS), significantly inhibits the growth of Escherichia coli in a dose-dependent manner. Further studies have shown that H2S treatment stimulates the production of reactive oxygen species (ROS) and decreases glutathione (GSH) levels in E. coli, resulting in lipid peroxidation and DNA damage. H2S also inhibits the antioxidative enzyme activities of superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) and induces the response of the SoxRS and OxyR regulons in E. coli. Moreover, pretreatment with the antioxidant ascorbic acid (AsA) could effectively prevent H2S-induced toxicity in E. coli. Taken together, our results indicate that H2S exhibits an antibacterial effect on E. coli through oxidative damage and suggest a possible application for H2S in water and food processing.

Epitaxial growth of <010>-oriented MoO2 nanorods on m-sapphire

Jinxin Liu,Jiao Shi,Di Wu,Xiaoming Zheng,Fengming Chen,Junting Xiao,Youzhen Li,Fei Song,Yongli Gao,Han Huang 한국물리학회 2020 Current Applied Physics Vol.20 No.10

Molybdenum dioxide (MoO2) materials have attracted considerable interests due to their superduper properties and potential applications, relating to the growth directions and exposed surfaces. Here, we reported as the substrate changes from c-to m-sapphire, the growth direction of epitaxial MoO2 nanorods via an atmospheric pressure chemical vapor deposition approach changes along from <001> to <010> of bulk monoclinic MoO2 accompanied by exposing different surfaces. Optical microscopy (OM), Raman spectroscopy, X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), cross-sectional scanning electron microscopy (SEM), highresolution transmission electron microscopy (HRTEM) and selected area electron diffraction (SAED) measurements reveal these MoO2 nanorods are epitaxially grown on m-sapphire substrates with the orientation of MoO2 (101)//sapphire (1010) and MoO2 <010> in line with sapphire <0001>. The electrical conductivity significantly depends on the crystallographic direction of MoO2 nanorods. The method to control the growth directions of 1D MoO2 nanorods has potential applications in nanoelectronic devices.

Kojic Acid Protects C57BL/6 Mice from Gamma-irradiation Induced Damage

Wang, Kai,Liu, Chao,Di, Chan-Juan,Ma, Cong,Han, Chun-Guang,Yuan, Mei-Ru,Li, Peng-Fei,Li, Lu,Liu, Yong-Xue Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.1

The radioprotective effects of a single administration of kojic acid (KA) against ionizing radiation were evaluated via assessment of 30-day survival and alterations of peripheral blood parameters of adult C57BL/6 male mice. The 30-day survival rate of mice pretreated with KA (75 or 300 mg/kg body weight, KA75 or KA300) subcutaneously 27 h prior to a lethal dose (8 Gy, 153.52 cGy/min) of gamma irradiation was higher than that of mice irradiated alone (40% or 60% vs 0%). It was observed that the white blood cell (WBC) count/the red blood cell (RBC) count, haemoglobin content, haematocrit and platelet count of mice with or without KA pretreatment as exposed to a sub-lethal dose (4 Gy, 148.14 cGy/min) of gamma irradiation decreased maximally at day 4/day 8 post-irradiation. Although the initial WBC values were low in KA300 or WR-2721 (amifostine) groups, they significantly recovered to normal at day 19, whereas in the control group they did not. The results from the cytotoxicity and cell viability assays demonstrated that KA could highly protect Chinese hamster ovary (CHO) cells against ionizing radiation with low toxicity. In summary, KA provides marked radioprotective effects both in vivo and in vitro.

SIRT5-related desuccinylation modification of AIFM1 protects against compression-induced intervertebral disc degeneration by regulating mitochondrial homeostasis

Mao Jianxin,Wang Di,Wang Dong,Wu Qi,Shang Qiliang,Gao Chu,Wang Huanbo,Wang Han,Du Mu,Peng Pandi,Jia Haoruo,Xu Xiaolong,Wang Jie,Yang Liu,Luo Zhuojing 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

Mitochondrial dysfunction plays a major role in the development of intervertebral disc degeneration (IDD). Sirtuin 5 (SIRT5) participates in the maintenance of mitochondrial homeostasis through its desuccinylase activity. However, it is still unclear whether succinylation or SIRT5 is involved in the impairment of mitochondria and development of IDD induced by excessive mechanical stress. Our 4D label-free quantitative proteomic results showed decreased expression of the desuccinylase SIRT5 in rat nucleus pulposus (NP) tissues under mechanical loading. Overexpression of Sirt5 effectively alleviated, whereas knockdown of Sirt5 aggravated, the apoptosis and dysfunction of NP cells under mechanical stress, consistent with the more severe IDD phenotype of Sirt5 KO mice than wild-type mice that underwent lumbar spine instability (LSI) surgery. Moreover, immunoprecipitation-coupled mass spectrometry (IP-MS) results suggested that AIFM1 was a downstream target of SIRT5, which was verified by a Co-IP assay. We further demonstrated that reduced SIRT5 expression resulted in the increased succinylation of AIFM1, which in turn abolished the interaction between AIFM1 and CHCHD4 and thus led to the reduced electron transfer chain (ETC) complex subunits in NP cells. Reduced ETC complex subunits resulted in mitochondrial dysfunction and the subsequent occurrence of IDD under mechanical stress. Finally, we validated the efficacy of treatments targeting disrupted mitochondrial protein importation by upregulating SIRT5 expression or methylene blue (MB) administration in the compression-induced rat IDD model. In conclusion, our study provides new insights into the occurrence and development of IDD and offers promising therapeutic approaches for IDD.

Patterns of Failure and Survival Trends in 3,808 Patients with Stage II Nasopharyngeal Carcinoma Diagnosed from 1990 to 2012: A Large-Scale Retrospective Cohort Study

Xue-Song Sun,Di-Han Liu,Sai-Lan Liu,Qiu-Yan Chen,Shan-Shan Guo,Yue-Feng Wen,Li-Ting Liu,Hao-Jun Xie,Qing-Nan Tang,Yu-Jing Liang,Xiao-Yun Li,Jin-Jie Yan,Ming-Huang Hong,Jun Ma,Lin-Quan Tang,Hai-Qiang M 대한암학회 2019 Cancer Research and Treatment Vol.51 No.4

Purpose The purpose of this study was to investigate the survival trends and patterns of failure in patients with stage II nasopharyngeal carcinoma (NPC) treated with radiotherapy (RT) and chemotherapy over the last 20 years. Materials and Methods Thirty-eight hundred and eight patients diagnosed with stage II NPC between January 1990 and December 2012 were involved in this retrospective cohort study. All patients were treated with RT. According to the main imaging techniques and RT technology, we categorized these patients into four calendar periods: 1990-1996, 1997-2002, 2003-2007, and 2008-2012. Overall survival (OS), progression-free survival (PFS), locoregional relapse-free survival (LRFS), and distant metastasis–free survival (DMFS) were served as the clinical outcome. Results After a median follow-up period of 84.7 months, we observed increasing trends in survival and disease control. The 3- and 5-year OS rates increased from 87.1% and 78.7% in the first calendar period to 97.4% and 94.5% in the last calendar period, respectively (p < 0.001). Additionally, significant increasing trends could be seen in the PFS and LRFS during the four calendar periods. In the subgroup analysis, the LRFS in patients older than 50 years at diagnosis showed greater improvement than younger patients. However, the rate of distant metastasis was stable and relatively low, as the 5-year DMFS ranged from 90.5% to 94.7% among the four calendar periods. Conclusion The survival rates in patients with stage II NPC showed increasing trends from 1990 to 2012. The advance of RT provided excellent locoregional control and enhanced OS.

Novel blood-based hypomethylation of SH3BP5 is associated with very early-stage lung adenocarcinoma

Qiao Rong,Zhong Runbo,Liu Chunlan,Di Feifei,Zhang Zheng,Wang Ling,Xu Tian,Wang Yue,Dai Liping,Gu Wanjian,Han Baohui,Yang Rongxi 한국유전학회 2022 Genes & Genomics Vol.44 No.4

Background: Early detection is essential to improve the survival of lung cancer (LC). The quantitative measurement of specific DNA methylation changes in the peripheral blood could provide an efficient strategy for the detection of early cancer. Objective: We applied a candidate approach and assess the association between blood-based SH3BP5 methylation and the risk of lung adenocarcinoma (LUAD) in a case-control cohort. Methods: The methylation level of four CpG sites in the promoter of SH3BP5 gene was quantitatively determined by mass spectrometry in 171 very early-stage LUAD patients (93.6% LUAD at stage I) and 190 age and gender-matched controls. The logistic regression and non-parametric tests were used for the statistical analyses. Results: We observed a significant association between decreased methylation of SH3BP5_CpG_4 in the peripheral blood and increased risk of LUAD (odds ratio (OR) per-10% methylation = 1.51, P = 0.006, FDR = 0.024), and even for the LUAD at stage I (OR per-10% methylation = 1.53, P = 0.006, FDR = 0.024). Moreover, the lower quartile of SH3BP5_CpG_4 methylation was correlated with increased risk for LUAD with a P trend of 0.011. Further investigation disclosed that the hypomethylation of SH3BP5_CpG_4 was mostly associated with LUAD in younger subjects (OR per-10% methylation = 2.02, P = 0.010, age < 55 years old) and probably could be enhanced by advance stage. Conclusion: Our study revealed an association between blood-based SH3BP5 hypomethylation and very early-stage LUAD, which provides a novel support for the blood-based methylation signatures as a potential marker for the evaluation of cancer risk.

Effect of cadmium exposure on antioxidant enzyme catalase in different tissues of Acrossocheilus fasciatus

Yong-Qiang Zhao,Guo-Di Liu,Cong-Cong Hou,Ying-Li Han,Jun-Quan Zhu,Jun-Quan Zhu 대한독성 유전단백체 학회 2016 Molecular & cellular toxicology Vol.12 No.3

Catalase (CAT) is an essential antioxidant in organisms, its can eliminate hydrogen peroxides produced in the cellular environment. Previous studies have focused mainly on the functions of CAT by pathogen challenge, but the functions of CAT by metals stress remain unclear. In order to investigate the function of CAT in Acrossocheilus fasciatus (AfCat), we cloned CAT complete cDNA sequences and analyzed its functions by cadmium (Cd) stress. qPCR analysis illustrated that the expression of CAT changed rapidly and dynamically in response to Cd from 0.05 mg L-1 to 1.25 mg L-1. Enzyme activity assay result showed that CAT activity was up-regulated significantly in response to Cd from 0.05 mg L-1 to 1.25 mg L-1. Histochemistry analysis showed that the structure of liver, testis and kidney were severely damaged by exposed to Cd of 1.25 mg L-1. Collectively, the results of our study indicate that AfCat may play an indispensable role in maintaining redox balance under Cd exposure, but AfCat expression will be inhibited when Cd accumulation reaches to the critical concentration. This study will illuminate the potential functions of AfCat in the defense mechanisms of reproductive and metabolic systems under Cd exposure in A. fasciatus.

Nicotine Induces the Expression of C-Reactive Protein via MAPK-Dependent Signal Pathway in U937 Macrophages

Junjun Mao,Juntian Liu,Xiaoming Pang,Ming Li,Jinyan Song,Chunjie Han,Di Wu,Shuyue Wang 한국분자세포생물학회 2012 Molecules and cells Vol.34 No.5

Atherosclerosis is an inflammatory disease in the vessel wall. Nicotine, a major component of cigarette smoke, is an independent risk factor for cardiovascular diseases including atherosclerosis. As an inflammatory molecule, C- reactive protein (CRP) participates in atherogenesis. Although it has been confirmed that CRP level in smoking patient is significantly higher than non-smokers and cigarette withdrawal,it is unknown whether nicotine induces CRP expression in macrophages. The present study was to observe effect of nicotine on CRP production and the related signal pathway in U937 macrophages. The results showed that nicotine significantly increased mRNA and protein expression of CRP in U937 macrophages in time- and concentration-dependent ways. Nicotinic acetylcholine receptor (nAChR) blocker hexamethonium, MEK1/2 inhibitor PD98059, p38 MAPK inhibitor SB203580 and NF-B inhibitor PDTC almost completely abolished nicotine-induced CRP expression in mRNA and protein levels in U937 macrophages. The further study indicated that hexa-methonium, PD98059, and SB203580 significantly inhibited ERK1/2 and p38 MAPK phosphorylation. These demonstrate that nicotine has ability to induce CRP ex-pression in macrophages through nAChR-ERK1/2/p38 MAPK-NF-B signal pathway, which contributes to better understanding of the pro-inflammatory and pro-atherosclerotic effects of nicotine in cigarette smokers.

Distribution and using of Medicinal Plant in Mt. Jangback (Baekdu)

Hu Lin Li(이호림),Ru Zi Piao,Di Liu,Jae Han Cho(조재한),Gi Hong An(안기홍),Won Sik Kong(공원식),Yun Ji Lee(이윤지),Jin Tae Jeong(정진태),Chun Geun Park(박춘근),Jeong Hoon Lee(이정훈),한재구 한국약용작물학회 2020 한국약용작물학회 학술대회논문집 Vol.2020 No.1