• 대한한방내과학회지
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• 제27권1호
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• pp.92-101
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• 2006

Objectives : This study was done with intend to investigate whether two oriental medical prescriptions, daecheongryong-tang (DCRT) and prescription A (P-A) significantly affect mucin release from cultured hamster tracheal surface epithelial (HTSE) cells. Methods : Confluent HTSE cells were metabolically radiolabeled with $^3H$-glucosamine for 24 hrs and chased for 30 min in the presence of DCRT or P-A to assess the effect of each agent on $^3H$-mucin release. Possible cytotoxicities of each agent were assessed by measuring lactate dehydrogenase (LDH) release. Also, the effects of DCRT and P-A on contractility of isolated tracheal smooth muscle were investigated. Results were as follows : 1. DCRT significantly inhibited mucin release from cultured HTSE cells, with significant cytotoxicity. 2. P-A significantly increased mucin release from cultured HTSE cells, with significant cytotoxicity. 3. DCRT inhibited Ach-induced contraction of isolated tracheal smooth muscle. 4. P-A also inhibited Ach-induced contraction of isolated tracheal smooth muscle. Conclusion: Results suggest that DCRT and P-A have regulating effects on mucin secretion from goblet cells. Further investigation is needed, because of the value in finding novel agents to this purpose, and these oriental medical prescriptions have potential for this role.

• 대한한방소아과학회지
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• 제24권3호
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• pp.92-105
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• 2010

Objectives: The purpose of this study is to investigate the effects of Daecheongryong-tang (DCRT) on the adipogenesis in 3T3-L1 preadipocytes. Methods: 3T3-L1 preadipocytes were differentiated with adipogenic reagents by incubating for 2 days in the absence or presence of DCRT ranging 0.25 and 2%. The effect of DCRT on adipogenesis was examined by Oil red O staining, and the protein, RNA, and RT-PCR were measured. Results: Our results showed that DCRT decreased the TG content by ORO staining. To elucidate the mechanism of the effects of DCRT on lowering TG content in 3T3-L1 adipocytes, we examined the DCRT modulate expressions of transcription factors to induce adipogenesis and adipogenic genes which is related to the regulation of accumulation of lipids. As a result, the expression of SREBP1, C/$EBP{\beta}$, C/$EBP{\delta}$, C/$EBP{\alpha}$, and $PPAR{\gamma}$ genes, which induce the adipose differentiation and adipose-specific aP2, adipsin, LPL, CD36, TGF-${\beta}$ and adiponectin genes which regulates fat formations, were decreased. In addition, DCRT reduced the expression of iNOS and IL-6 in 3T3-L1 adipocytes, resulting in inflammation. Conclusions: DCRT could regulate transcript factor related to induction of adipose differentiation, inhibit the accumulation of lipids and expression of the adipogenic genes.