Presentation Information
[P02-181]JMB326 Alleviates UV-induced Pruritus, Pain and Skin Damage via Downregulating mPGES1 and Other Inflammatory Mediators
○Jun Li1,2, Yue Wang1,2, Yutian Bao2, Yue Zou1 (1. Shanghai CHANDO Group Co., Ltd. (China), 2. Himalaya Third Pole (Shanghai) Biotechnology Co., Ltd. (China))
Keywords:
Photo-protection,Skin care,Pain reduction,Fermentation,mPGES1
[Purpose]
In daily life, human skin is continually exposed to a range of external environmental stressors, often without conscious awareness. Ultraviolet (UV) radiation remains the most extensively studied and clinically significant exogenous stressor in dermatological research and skincare practice. Chronic or acute UV exposure triggers cutaneous inflammatory responses, clinically characterized by erythema, pruritus, epidermal desquamation, and, in severe cases, pain.The enzymes cPLA2 and mPGES1 can be activated by ultraviolet light, thereby increasing PGE2 production by keratinocytes. PGE2, LTB4, TSLP, and IL-17α are considered inflammatory mediators associated with skin itching and pain.Therefore, JMB326, a raw material sourced from the Himalayas in China, can target and block the itch-pain pathway, repair the skin barrier, and help patients address the urgent problem of pain and itching while also maintaining skin barrier health.
[Method]
Human keratinocytes were used and exposed to UVB to create an UV damage model. Cell viability was assessed using the CCK-8 kit, and the mRNA expression levels of inflammatory and pain-related factors in the cells were measured by qPCR. PGE2 content was calibrated using ELISA.
[Results]
At an addition concentration of 5% (v/v), JMB326 can effectively prevent the damage caused by UVA and UVB to fibroblasts and keratinocytes; it can increase the expression of HSP60 in HaCAT cells by 195% (p<0.001); JMB326 can down-regulate the mRNA expression levels of factors related to inflammation, itching and pain, such as IL-17α, IL6, caspase-1, cPLA2, mPGES1, LTA4H, in keratinocytes. It was found that at an additional concentration of 5% (v/v), JMB326 effectively downregulates PGE2 expression in keratinocytes by 42.9% (p<0.001).
[Consideration]
The research results show that JMB326 can help keratinocytes resist the damaging effects of UVB and, at the same time, effectively reduce the expression levels of inflammatory and pain-related cytokine mRNAs. The cPLA2 and mPGES1 pathways are the main routes for synthesizing PGE2. JMB326 can specifically regulate these two targets, and ELISA also revealed a significant decrease in PGE2 content. And the cPLA2 and mPGES1 signaling pathways are commonly used in cancer pain research, whereas there are few reports on their applications in the development of skincare raw materials. This is a very transformative exploration and discovery.
[Conclusion]
Using an in vitro keratinocyte model stimulated by UV radiation, the significant potential of JMB326 for photoprotection and anti-inflammatory analgesia was successfully discovered. This discovery indicates that JMB326 can be utilized in sunscreen and post-sun-exposure repair skincare products and also has potential applications in medical post-treatment repair products.
In daily life, human skin is continually exposed to a range of external environmental stressors, often without conscious awareness. Ultraviolet (UV) radiation remains the most extensively studied and clinically significant exogenous stressor in dermatological research and skincare practice. Chronic or acute UV exposure triggers cutaneous inflammatory responses, clinically characterized by erythema, pruritus, epidermal desquamation, and, in severe cases, pain.The enzymes cPLA2 and mPGES1 can be activated by ultraviolet light, thereby increasing PGE2 production by keratinocytes. PGE2, LTB4, TSLP, and IL-17α are considered inflammatory mediators associated with skin itching and pain.Therefore, JMB326, a raw material sourced from the Himalayas in China, can target and block the itch-pain pathway, repair the skin barrier, and help patients address the urgent problem of pain and itching while also maintaining skin barrier health.
[Method]
Human keratinocytes were used and exposed to UVB to create an UV damage model. Cell viability was assessed using the CCK-8 kit, and the mRNA expression levels of inflammatory and pain-related factors in the cells were measured by qPCR. PGE2 content was calibrated using ELISA.
[Results]
At an addition concentration of 5% (v/v), JMB326 can effectively prevent the damage caused by UVA and UVB to fibroblasts and keratinocytes; it can increase the expression of HSP60 in HaCAT cells by 195% (p<0.001); JMB326 can down-regulate the mRNA expression levels of factors related to inflammation, itching and pain, such as IL-17α, IL6, caspase-1, cPLA2, mPGES1, LTA4H, in keratinocytes. It was found that at an additional concentration of 5% (v/v), JMB326 effectively downregulates PGE2 expression in keratinocytes by 42.9% (p<0.001).
[Consideration]
The research results show that JMB326 can help keratinocytes resist the damaging effects of UVB and, at the same time, effectively reduce the expression levels of inflammatory and pain-related cytokine mRNAs. The cPLA2 and mPGES1 pathways are the main routes for synthesizing PGE2. JMB326 can specifically regulate these two targets, and ELISA also revealed a significant decrease in PGE2 content. And the cPLA2 and mPGES1 signaling pathways are commonly used in cancer pain research, whereas there are few reports on their applications in the development of skincare raw materials. This is a very transformative exploration and discovery.
[Conclusion]
Using an in vitro keratinocyte model stimulated by UV radiation, the significant potential of JMB326 for photoprotection and anti-inflammatory analgesia was successfully discovered. This discovery indicates that JMB326 can be utilized in sunscreen and post-sun-exposure repair skincare products and also has potential applications in medical post-treatment repair products.
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