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Kang, Sohi,Yang, Wonjun,Oh, Hanseul,Bae, Yeonji,Ahn, Meejung,Kang, Min Chul,Ko, Ryeo Kyeong,Kim, Gi Ok,Lee, Jun Hwa,Hyun, Jin Won,Moon, Changjong,Shin, Taekyun The Korean Society of Veterinary Science 2011 大韓獸醫學會誌 Vol.51 No.4
Several compounds and extracts isolated from a brown alga, Ishige (I.) okamurae, exhibit anti-oxidant and anti-inflammatory effects. The present study investigated whether the ethyl acetate (EtOAc) fraction of I. okamurae (EFIO) could ameliorate carbon tetrachloride ($CCl_{4}$)-induced hepatotoxicity in rats. Sprague-Dawley rats were intraperitoneally (i.p.) administered with EFIO at 10 or 50 mg/kg per day for 2 consecutive days before $CCl_{4}$ injection (3.3 mL/kg, i.p.). Twenty four hours later, the rats were anesthesized with diethyl ether and dissected. Pretreatment with EFIO significantly reduced the increased serum levels of alanine aminotransferase and aspartate aminotransferase in $CCl_{4}$-treated rats. Pretreatment with EFIO also significantly inhibited the reduced activities of superoxide dismutase and catalase in the $CCl_{4}$-injured liver. Histopathological evaluations showed that hemorrhage, hepatocyte necrosis, inflammatory cell infiltration, and fatty degeneration induced by $CCl_{4}$ treatment were ameliorated by the administration of EFIO. Additionally, liver immunohistochemical analyses revealed the marked reduction in ED1-positive monocyte-like macrophages in EFIO-pretreated rats given $CCl_{4}$. These results suggest that EFIO ameliorates $CCl_{4}$-induced liver injury, possibly through the inhibition of oxidative stress.
강소희 ( Sohi Kang ),이수은 ( Su Eun Lee ),이아영 ( Ayeong Lee ),서윤수 ( Yun-soo Seo ),문창종 ( Changjong Moon ),김성호 ( Sung Ho Kim ),이지혜 ( Jihye Lee ),김중선 ( Joong Sun Kim ) 대한본초학회 2021 大韓本草學會誌 Vol.36 No.6
Objectives : Atractylodis rhizoma Alba has been traditionally used as a medicinal resource that is used for enhancing Qi (氣) in traditional medicine in Korea, China, and Japan. This study investigated the protective effects of Atractylodis rhizoma Alba extract (ARE) against trimethyltin (TMT), a neurotoxin that causes selective hippocampal injury, using both in vitro and in vivo models. Methods : We investigated the effects of ARE on TMT- (5mM) induced cytotoxicity in primary cultures of mouse hippocampal cells (7 days in vitro ) and on hippocampal injury in C57BL/6 mice injected with TMT (2.6 mg/kg). Results : We observed that ARE treatment (0 - 50 μg/mL) significantly reduced TMT-induced cytotoxicity in cultured hippocampal neurons in a dose-dependent manner, based on results of lactate dehydrogenase and 3-4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide assays. Additionally, this study showed that orally administered ARE (5 mg/kg; between -6 and 0 days before TMT injection) significantly attenuated seizures in adult mice. Furthermore, quantitative analysis of allograft inflammatory factor-1 (Iba-1)- and glial fibrillary acidic protein (GFAP)- positive cells showed significantly reduced levels of Iba-1- and GFAP-positive cell bodies in the dentate gyrus of mice treated with ARE prior to TMT injection. These findings indicate the significant protective effects of ARE against the TMT-induced massive activation of microglia and astrocytes in the hippocampus. Conclusions : We conclude that ARE minimizes the detrimental effects of TMT-induced hippocampal neurotoxicity, both in vitro and in vivo . Our findings may serve as useful guidelines to support ARE administration as a promising pharmacotherapeutic approach to hippocampal degeneration.
Kang, Sohi,Son, Yeonghoon,Lee, Sueun,Kim, Juhwan,Kim, Jong-Choon,Kim, Joong-Sun,Jung, Uhee,Kim, Sung-Ho,Yang, Miyoung,Moon, Changjong Elsevier/North-Holland 2017 Neuroscience letters Vol.657 No.-
<P><B>Abstract</B></P> <P>Brain exposure to ionizing radiation can cause functional deficits in the hippocampus, including memory impairment. However, the specific molecular mechanisms underlying irradiation-induced cognitive impairments are largely unknown. Changes in DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), which are involved in DNA methylation and histone remodeling, may be associated with behavioral changes in learning and memory. We assessed changes in the levels of enzymes associated with the epigenetic modification of gene expression, including DNMT1, HDAC1, HDAC2, Sirtuin 1 (SIRT1), and acetylated histone H3 (Ace-H3) in the mouse hippocampus 1 and 30days after a single exposure to cranial irradiation (0 or 10Gy). mRNA levels of HDAC1 were significantly downregulated 1day after irradiation with 10Gy, and those of DNMT1, HDAC1, and HDAC2 were significantly downregulated 30days post-irradiation. Western blot analysis revealed significant decreases in DNMT1, HDAC1, and HDAC2 protein levels 1 and 30days after irradiation with 10Gy. Furthermore, protein levels of SIRT1 and Ace-H3 were significantly downregulated in the mouse hippocampus 1 and 30days after cranial irradiation. Our findings suggest that the reduction in epigenetic gene expression is associated with hippocampal dysfunction in mice exposed to cranial irradiation.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Epigenetic modification plays an important role during hippocampal memory processing. </LI> <LI> Cranial irradiation inhibited hippocampal epigenetic modification signals in mice. </LI> <LI> Decreased epigenetic modification signals may be involved in radiation-induced hippocampal dysfunctions. </LI> </UL> </P>
Low-dose-rate gamma radiation aggravates titanium dioxide nanoparticle-induced lung injury in mice
Kang Sohi,Lee Hae-June,Son Yeonghoon,Bae Min Ji,Jo Wol Soon,Park Jun Hong,Jeong Sohee,Moon Changjong,Shin In-Sik,Lee Chang Geun,Kim Joong-Sun 대한독성 유전단백체 학회 2024 Molecular & cellular toxicology Vol.20 No.2
Background Radiation damage and the cellular response has been studied in various direction, however, the synergic effects of radiation damage with environmental pollution on cells or tissues remained poorly understood. In particular, gene and pathway regulation by low-dose radiation exposure remains unclear. Dust and air pollution in Asian countries contains metal oxide and titanium dioxide nanoparticles (TiO2NPs), which exacerbate respiratory distress. Objective To explore the synergic injury of radiation damage with air pollution, we examined the effects of low-dose-rate radiation with TiO2NPs on pulmonary response in mice. Results Thirty-six mice (C57bl/6) were divided into six groups: sham, 0.1 Gy, 0.3 Gy, TiO2NPs, TiO2NPs + 0.1 Gy, and TiO2NPs + 0.3 Gy group. Mice were irradiated at a low-dose-rate at a dose of 0.1 Gy (0.182 mGy/h) and 0.3 Gy (0.554 mGy/h) for 24 days and exposed to TiO2NPs by intranasal injection at a dose of 0.1 mg daily for 4 days (from day 21 to 24). The combination of low-dose-rate radiation and TiO2NPs caused significantly more pulmonary inflammation via MAPK phosphorylation in mice than did each stimulus alone. Conclusion We conclude that while exposure to each of these two distinct stimuli alone does not cause notable lung damage, they may potentially cause lung damage when combined owing to their synergistic effects. Therefore, we should pay attention to the possible combined effects of low-dose radiation and exposure to TiO2NPs, considering their potential danger in patients with respiratory problems.
Appearance of osteoporosis in rat experimental autoimmune encephalomyelitis
Ahn, Meejung,Kang, Sohi,Park, Channam,Kim, Jeongtae,Jung, Kyungsook,Yang, Miyoung,Kim, Sung-Ho,Moon, Changjong,Shin, Taekyun The Korean Society of Veterinary Science 2016 大韓獸醫學會誌 Vol.56 No.2
Experimental autoimmune encephalomyelitis (EAE) in Lewis rats is characterized by transient paralysis followed by recovery. To evaluate whether transient paralysis in EAE affects bone density, tibiae of EAE rats were morphologically investigated using micro-computed tomography and histology. The parameters of bone health were significantly reduced at the peak stage of EAE rats relative to those of controls (p < 0.05). The reduction of bone density was found to remain unchanged, even in the recovery stage. Collectively, the present data suggest that osteoporosis occurs in paralytic rats with monophasic EAE, possibly through the disuse of hindlimbs and/or autoimmune inflammation.