• The Journal of Pediatrics of Korean Medicine
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• v.34 no.3
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• pp.67-75
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• 2020

Objectives This study is conducted to evaluate Th2 skewed condition control through skin fat barrier formation from the treatment using Coptidis Rhizoma and Glycyrrhiza uralensis extract. Methods The 6-week-old NC/Nga mice were divided into 4 groups: Control group (Ctrl), lipid barrier eliminate treatment group (LBET), Coptidis Rhizoma and Glycyrrhiza uralensis feeding treatment after lipid barrier elimination group (CGFT), dexamethasone feeding treatment after lipid barrier elimination group (DxFT). After 3 days, differences in skin condition, improvement of skin fat barrier, and control of Th2 skewed condition of each group were observed. Results Pathologic skin damage and tissue changes were less in the CGFT group than in the LBET and DxFT groups, and Transepidermal water loss (TEWL) and pH were also significantly decreased (p < 0.05). The filaggrin intensity and positive response also increased significantly in the CGFT group (p < 0.05). Kallikrein-related peptidase (KLK) 7, Protease activated receptor (PAR)-2, Thymic stromal lymphopoietin (TSLP), Interleukin (IL)-4, and the products of the Th2 differentiation process also showed a significant decrease compared to the LBET and DxFT groups (all p < 0.05). Conclusions The Coptidis Rhizoma and Glycyrrhiza uralensis extract causes skin barrier recovery and function recovery through the formation of skin fat barrier. This leads to the conclusion that Coptidis Rhizoma and Glycyrrhiza uralensis extract can control Th2 differentiation through the formation of skin fat barrier.

• Journal of Ginseng Research
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• v.32 no.2
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• pp.107-113
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• 2008

In this study, we have investigated the effect of panaxatriol (PT) on phosphoinositides (PIS) breakdown and $Ca^{2+}$-elevation in thrombin-induced platelet aggregation. Thrombin (5U/ml), a potent platelet agonist which activates phospholipase $C_{\beta}$ via protease activated receptor (PAR), hydrolyzed PIS in platelet membrane. The phosphatidylinositol 4, 5-bisphosphate $(PIP_2)$ was hydrolyzed after 10 sec of the thrombin-stimulation, and both the phosphatidylinositol 4-monophosphate (PIP) and phosphatidylinositol (PI) were brokendown after 30 sec of the thrombin-stimulation. However, PT inhibited the thrombin-stimulated hydrolysis of $PIP_2$, PIP, and PI. On the other hand, thrombin increased the level of phosphatidic acid (PA) which is phosphorylated from diacylglycerol (DG) generated by PIS-hydrolysis. However, Pr inhibited the thrombin-increased PA level non-significantly. Thrombin increased cytosolic free $Ca^{2+}([Ca^{2+}])_i$) up to 72% as compared with control $(30.8{\pm}0.9 nM)$ in intact platelet. However, PT (100 ${\mu}g/ml$) inhibited the thrombin-elevated $[Ca^{2+}]_i$ to 100%. These results suggest that PT may have a beneficial effect on platelet aggregation-mediated thrombotic disease by inhibiting thrombin-induced platelet aggregation via suppression of the $[Ca^{2+}]_i$ level and PIS breakdown.