• 제목/요약/키워드: Hwang Kyung-Ha

검색결과 381건 처리시간 0.03초

Particulate Matter-Induced Aryl Hydrocarbon Receptor Regulates Autophagy in Keratinocytes

  • Jang, Hye sung;Lee, Ji eun;Myung, Cheol hwan;Park, Jong il;Jo, Chan song;Hwang, Jae Sung
    • Biomolecules & Therapeutics
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    • 제27권6호
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    • pp.570-576
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    • 2019
  • Particulate matter (PM), which refers to the mixture of particles present in the air, can have harmful effects. Damage to cells by PM, including disruption of organelles and proteins, can trigger autophagy, and the relationship between autophagy and PM has been well studied. However, the cellular regulators of PM-induced autophagy have not been well characterized, especially in keratinocytes. The Aryl Hydrocarbon Receptor (AhR) is expressed in the epidermis and is activated by PM. In this study, we investigated the role of the AhR in PM-induced autophagy in HaCaT cells. Our results showed that PM led to AhR activation in keratinocytes. Activation of the AhR-target gene CYP1A1 by PM was reduced by co-treatment with ${\alpha}$-naphthoflavone (${\alpha}-NF$), an AhR inhibitor. We also evaluated activation of the autophagy pathway in PM-treated keratinocytes. In HaCaT cells, treatment with PM treatment led to the induction of microtubules-associated proteins light chain 3 (LC3) and p62/SQSTM1, which are essential components of the autophagy pathway. To study the role of the AhR in mediating PM-induced autophagy, we treated cells with ${\alpha}-NF$ or used an siRNA against AhR. Expression of LC3-II induced by PM was decreased in a dose dependent manner by ${\alpha}-NF$. Furthermore, knockdown of AhR with siAhR diminished PM-induced expression of LC3-II and p62. Together, these results suggest that inhibition of the AhR decreases PM-induced autophagy. We confirmed these results using the autophagy-inhibitors BAF and 3-MA. Taken together, our results indicate that exposure to PM induces autophagy via the AhR in HaCaT keratinocytes.

인후부 이물감 호소에 따른 위식도역류질환 환자의 임상적 특징 비교 (Comparison of the Clinical Characteristics of Patients with Gastroesophageal Reflux Disease According to Globus Sensation)

  • 백소영;황미니;고휘형;김동윤;이하늘;정해인;하나연;김진성
    • 대한한방내과학회지
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    • 제40권3호
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    • pp.287-294
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    • 2019
  • Objectives: This study aimed to investigate the clinical characteristics of patients with gastroesophageal reflux disease (GERD) according to globus sensation (GS). Methods: We reviewed the clinical records of 29 GERD patients who visited the Department of Digestive Diseases of Kyung Hee University Korean Medicine Hospital from March 1, 2018 to February 28, 2019. The subjects were classified according to the presence of globus sensation, and the two groups were compared in terms of heart rate variability (HRV) and the Ryodoraku results. Results: In comparing the GERD with GS group (GS group) and the GERD without GS group (non-GS group), a significant difference was found in the duration of symptom and several HRV parameters. The duration of the symptom in the GS group was significantly longer than that in the non-GS group. The non-GS group showed a significantly higher value of total power and high frequency than the GS group. Conclusions: The results suggest a significant difference in the stress level between patients with GERD with GS and those without GS. When approaching patients with GERD without GS, their stress status should be considered.

미만성 식도경련의 한방 치료 : 증례보고 (Case Study of Korean Medicine Treatment of Diffuse Esophageal Spasm)

  • 김동윤;황미니;고휘형;백소영;이하늘;정해인;하나연;김진성
    • 대한한방내과학회지
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    • 제40권5호
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    • pp.814-821
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    • 2019
  • Objective: This case study reports on the result of Korean medicine treatment of diffuse esophageal spasm. Methods: A 46-year-old female Korean patient with diffuse esophageal spasm received electroacupuncture, herbal medicine, and moxibustion treatment for 2 weeks in hospital. Results: Decreases in the visual analog scale (VAS) (from 8.7 to 7.0), numeric rating scale (NRS) (from 7.0 to 5.5), gastrointestinal symptom rating scale (GSRS) (from 9 to 6), and gastroesophageal reflux disease-health related quality of life questionnaire (GERD-HRQL) (from 46 to 38) scores were observed after the treatment. Conclusion: Evaluation of Korean medicine treatment is worthwhile for rare diseases like diffuse esophageal spasm.

Impact on Inflammation and Recovery of Skin Barrier by Nordihydroguaiaretic Acid as a Protease-Activated Receptor 2 Antagonist

  • Kim, Hyo-Young;Goo, Jung-Hyun;Joo, Yeon-Ah;Lee, Ha-Yoen;Lee, Se-Mi;Oh, Chang-Taek;Ahn, Soo-Mi;Kim, Nam-Hoon;Hwang, Jae-Sung
    • Biomolecules & Therapeutics
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    • 제20권5호
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    • pp.463-469
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    • 2012
  • Atopic dermatitis is a chronic, inflammatory disease of the skin with increased transepidermal water loss. Both an abnormal inflammatory response and a defective skin barrier are known to be involved in the pathogenesis of atopic dermatitis. Protease activated receptor 2 (PAR2) belongs to a family of G-protein coupled receptors and is activated by both trypsin and a specific agonist peptide, SLIGKV-$NH_2$. PAR2 is expressed in suprabasal layers of the epidermis and regulates inflammatory responses and barrier homeostasis. In this study, we show that nordihydroguaiaretic acid (NDGA) inhibits the PAR2-mediated signal pathway and plays a role in skin barrier recovery in atopic dermatitis. Specifically, NDGA reduces the mobilization of intracellular $Ca^{2+}$ in HaCaT keratinocytes by down-regulating inflammatory mediators, such as interleukin-8, thymus and activation-regulated chemokine and intercellular cell adhesion molecule-1 in HaCaT keratinocytes. Also, NDGA decreases the protein expression of involucrin, a differentiation maker of keratinocyte, in both HaCaT keratinocytes and normal human epidermal keratinocytes. We examined NDGA-recovered skin barrier in atopic dermatitis by using an oxazolone-induced atopic dermatitis model in hairless mice. Topical application of NDGA produced an increase in transepidermal water loss recovery and a decrease in serum IgE level, without weight loss. Accordingly, we suggest that NDGA acts as a PAR2 antagonist and may be a possible therapeutic agent for atopic dermatitis.