• Journal of the Society of Cosmetic Scientists of Korea
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• v.49 no.1
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• pp.87-96
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• 2023

This study was conducted to discover substances that regulate skin surface acidification using human epidermal keratinocyte cell lines, and to investigate their effects on the moisturizing ability and skin barrier function of the stratum corneum. Prunella vulgaris (P. vulgaris) is an herb widely distributed in Northwest Africa and North America that has been studied for its anti-apoptotic, antioxidant, and anti-inflammatory effects. However, research on the regulation of NHE1 expression and the restoration of skin barrier function has not been conducted. Analysis of P. vulgaris revealed the presence of rosmarinic acid and caffeic acid as active ingredients, which were tested for toxicity in human epidermal keratinocyte cell lines (HaCaT), and showed no toxic effects were observed at high concentarion (100 ㎍/mL or 100 µM). It is known that sodium-hydrogen ion exchange pumps (NHE1) decrease in expression in aging skin to maintain the acidic pH of the stratum corneum, and it is hypothesized that this decrease plays an important role in the impaired restoration of skin barrier function in aging skin. P. vulgaris extract and caffeic acid increased the expression of NHE1 in keratinocytes, increased the expression of natural moisturizing factor (NMF) precursor filaggrin and ceramide synthesis enzyme serine palmitoyl transferase (SPT). In addition, P. vulgaris and caffeic acid decreased the extracellular pH of keratinocytes, indicating a direct effect on skin pH regulation. Taken together, these results suggest that P. vulgaris and caffeic acid can regulate skin pH through NHE1 modulation, and may help to restore skin barrier function by increasing NMF and ceramide synthesis. These results show the possibility that honeysuckle and caffeic acid can have a positive effect on skin health, and can be the basis for the development of new skin protection products using them.

• Archives of Pharmacal Research
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• v.29 no.5
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• pp.375-383
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• 2006

The anti platelet effects of a novel guanidine derivative, KR-32570 ([5-(2-methoxy-5-chlorophenyl) furan-2-ylcarbonyl]guanidine), were investigated with an emphasis on the mechanisms underlying its inhibition of collagen-induced platelet aggregation. KR-32570 significantly inhibited the aggregation of washed rabbit platelets induced by collagen $(10{\mu}g/mL)$, thrombin (0.05 U/mL), arachidonic acid $(100{\mu}M)$, a thromboxane (TX) $A_2$ mimetic agent U46619 (9,11-dideoxy-9,11-methanoepoxy-prostaglandin $F_2,\;1{\mu}M$) and a $Ca^{2+}$ ATPase inhibitor thapsigargin $(0.5{\mu}M)$ ($IC_{50}$ values: $13.8{\pm}1.8,\;26.3{\pm}1.2,\;8.5{\pm}0.9,\;4.3{\pm}1.7\;and\;49.8{\pm}1.4{\mu}M$, respectively). KR-32570 inhibited the collagen-induced liberation of $[^3H]$arachidonic acid from the platelets in a concentration dependent manner with complete inhibition being observed at $50{\mu}M$. The $TXA_2$ synthase assay showed that KR-32570 also inhibited the conversion of the substrate $PGH_2$ to $TXB_2$ at all concentrations. Furthermore, KR-32570 significantly inhibited the $[Ca^{2+}]_i$ mobilization induced by collagen at $50{\mu}M$, which is the concentration that completely inhibits platelet aggregation. KR-32570 also decreased the level of collagen $(10{\mu}g/mL)$induced secretion of serotonin from the dense-granule contents of platelets, and inhibited the NHE-1-mediated rabbit platelet swelling induced by intracellular acidification. These results suggest that the antiplatelet activity of KR-32570 against collagen-induced platelet aggregation is mediated mainly by inhibiting the release of arachidonic acid, $TXA_2$ synthase, the mobilization of cytosolic $Ca^{2+}$ and NHE-1.