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Ko, Je-Won,Shin, Na-Rae,Jung, Tae-Yang,Shin, In-Sik,Moon, Changjong,Kim, Sung-Ho,Lee, In-Chul,Kim, Sung-Hwan,Yun, Won-Kee,Kim, Hyoung-Chin,Kim, Jong-Choon Elsevier 2019 Food and chemical toxicology Vol.129 No.-
<P><B>Abstract</B></P> <P>This study investigated the protective effects of melatonin (MT) against cisplatin (CP)-induced acute kidney injury in rats as well as its possible mechanism of action associated with anti-aging protein Klotho. The following four experimental groups were evaluated: vehicle control, CP (7 mg/kg), CP&MT20 (20 mg/kg/day), and CP&MT40 (40 mg/kg/day). The concomitant administration of MT significantly ameliorated CP-induced acute kidney injury in rats, as evidenced by increased kidney weight, increased serum levels of blood urea nitrogen and creatinine, and increased incidence of histopathological alterations with renal tubular cell apoptosis. In addition, MT treatment protected kidney tissue against oxidative damages and significantly upregulated the expression level of Klotho decreased by CP treatment, resulting in reduced phosphorylation of protein kinase B (AKT) and forkhead box O (FOXO) as well as reduced expression levels of B-cell lymphoma 2-associated X protein (Bax) and caspase-3. MT not only partially regulated oxidative stress via AKT/FOXO signaling, but also reduced apoptosis caused by CP by inhibiting the Bax/caspase-3 pathway. Our results indicated that MT could prevent acute kidney injury induced by CP in rats, presumably through upregulating the expression of Klotho, resulting in elevated anti-oxidant and anti-apoptotic properties.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Melatonin (MT) attenuated acute kidney injury induced by cisplatin (CP). </LI> <LI> MT upregulated the expression level of Klotho decreased by CP treatment. </LI> <LI> Upregulated Klotho attenuated oxidative stress and apoptosis induced by CP. </LI> </UL> </P>
Ko, Je-Won,Shin, Na-Rae,Park, Sung-Hyeuk,Lee, In-Chul,Ryu, Jung-Min,Kim, Ha-Jung,Cho, Young-Kwon,Kim, Jong-Choon,Shin, In-Sik Elsevier 2017 Food and Chemical Toxicology Vol. No.
<P><B>Abstract</B></P> <P>Cigarette smoke (CS) is generally accepted as a major contributor to chronic obstructive pulmonary disease (COPD) which is characterized by chronic inflammation, fibrotic response, and airway obstruction. In this study, we investigated the preventive effects of silibinin, an active constitute of silymarin on CS and lipopolysaccharide (LPS) exposure-induced fibrotic response. Mice were exposed to CS for 1 h per day (8 cigarettes per day) for 4 weeks. On day 12 and 26, mice were treated with LPS intranasally. Silibinin (10 or 20 mg/kg) was administered orally 1 h before CS exposure. Silibinin markedly decreased the inflammatory cell count in the bronchoalveolar lavage fluid, and reduced levels of proinflammatory mediators. Silibinin suppressed CS + LPS-induced collagen deposition in lung tissue, as evidenced via immunohistochemistry and Masson's trichrome stain. Additionally, silibinin effectively inhibited CS + LPS-mediated expression of transforming growth factor-β1 (TGF-β1) and Smad 2/3 phosphorylation. Taken together, our data indicate that silibinin effectively inhibits the fibrotic response induced by CS + LPS exposure, possibly via suppression of TGF-β1/Smad 2/3 signaling, which results in reduced collagen deposition. These findings suggest that silibinin has therapeutic potential for the treatment of COPD.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Protective effect of silibinin on airway fibrotic responses was investigated. </LI> <LI> Silibinin inhibited inflammatory responses. </LI> <LI> Silibinin inhibited collagen deposition, which was closely related to downregulation of TGF-β1/Smad 2/3 signaling. </LI> </UL> </P>
Genipin inhibits allergic responses in ovalbumin-induced asthmatic mice
Ko, Je-Won,Shin, Na-Rae,Park, Sung-Hyeuk,Cho, Young-Kwon,Kim, Jong-Choon,Seo, Chang-Seob,Shin, In-Sik ELSEVIER 2017 INTERNATIONAL IMMUNOPHARMACOLOGY Vol.53 No.-
<P><B>Abstract</B></P> <P>Genipin is a natural compound isolated from the fruit of <I>Gardenia jasminoides</I> with various pharmacological effects. In this study, we investigated whether genipin effectively alleviates allergic responses in a murine model of ovalbumin (OVA)-induced asthma. The mice were administered an intraperitoneal injection of OVA on day 0 and 14 to boost the immune response; genipin was then administered from day 18 to 23 by oral gavage. On days 21 to 23, mice were OVA-challenged using am ultrasonic nebulizer, and airway hyperresponsiveness (AHR) was determined on day 24 by plethysmography. Genipin significantly reduced the inflammatory cell count in bronchoalveolar lavage fluids (BALF) and AHR, which were accompanied by lower interleukin-5 (IL-5), IL-13 and OVA-specific immunoglobulin (Ig) E levels in the BALF or serum from OVA-induced asthmatic mice. In histology, genipin significantly decreased airway inflammation and mucus hypersecretion in OVA-induced asthmatic mice. Additionally, genipin inhibited OVA-induced increases in the expression of inducible nitric oxide synthase and cyclooxygenase-2 proteins. Further, genipin reduced the activity and protein levels of matrix metalloproteinase-9 in lung tissue from OVA induced asthmatic mice. Overall, genipin effectively alleviated the asthmatic inflammatory response in an OVA-induced asthmatic model. Therefore, our results suggest that genipin has therapeutic potential for treating asthma.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Effects of genipin on ovalbumin (OVA)-induced asthmatic mice </LI> <LI> Genipin decreased airway hyperresponsiveness and eosinophilia in asthmatic mice </LI> <LI> Genipin reduced IL-5, IL-13 and OVA-specific IgE in asthmatic mice </LI> <LI> Genipin suppressed airway inflammation and mucus production in asthmatic mice </LI> <LI> Genipin inhibited iNOS, COX-2 and MMP-9 in lung tissue from asthmatic mice </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Ko, Je-Won,Shin, Na-Rae,Park, Sung-Hyeuk,Kim, Joong-Sun,Cho, Young-Kwon,Kim, Jong-Choon,Shin, In-Sik,Shin, Dong-Ho Korean Association for Laboratory Animal Science 2017 Laboratory Animal Research Vol.33 No.2
<P>Chronic obstructive pulmonary diseases (COPD) is an important disease featured as intense inflammation, protease imbalance, and air flow limitation and mainly induced by cigarette smoke (CS). In present study, we explored the effects of Pycnogenol® (PYC, pine bark extract) on pulmonary fibrosis caused by CS+lipopolysaccharide (LPS) exposure. Mice were treated with LPS intranasally on day 12 and 26, followed by CS exposure for 1 h/day (8 cigarettes per day) for 4 weeks. One hour before CS exposure, 10 and 20 mg/kg of PYC were administered by oral gavage for 4 weeks. PYC effectively reduced the number of inflammatory cells and proinflammatory mediators caused by CS+LPS exposure in bronchoalveolar lavage fluid. PYC inhibited the collagen deposition on lung tissue caused by CS+LPS exposure, as evidenced by Masson's trichrome stain. Furthermore, transforming growth factor-β1 (TGF-β1) expression and Smad family member 2/3 (Smad 2/3) phosphorylation were effectively suppressed by PYC treatment. PYC markedly reduced the collagen deposition caused by CS+LPS exposure, which was closely involved in TGF-β1/Smad 2/3 signaling, which is associated with pulmonary fibrotic change. These findings suggest that treatment with PYC could be a therapeutic strategy for controlling COPD progression.</P>