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Background <p>Ultraviolet B (UVB) radiation disrupts skin homeostasis through reactive oxygen species (ROS)-mediated oxidative stress and melanogenic imbalance. The search for effective exogenous photoprotectants has highlighted natural products, including <i>Cannabis sativa</i> L. phytocannabinoids with reported antioxidant activity. However, their role in UVB-induced cellular responses remains to be clarified.</p> Methods <p>Chemical profiling was performed using LC-QTOF-MS and Fourier-transform infrared (FTIR) spectroscopy. Biological activities were assessed in B16-F10 pigmented melanoma cells, including cytotoxicity (MTT assay), intracellular ROS generation (DCFDA assay), transcriptional regulation of melanogenic markers (<i>MITF</i>, <i>TYR</i>, <i>TYRP1</i>, <i>TYRP2</i>) by RT-qPCR, and functional melanogenesis outcomes (tyrosinase activity and melanin content).</p> Results <p>LC-QTOF-MS revealed that the extract was dominated by neutral cannabinoids, with Δ⁹-tetrahydrocannabinol (Δ⁹-THC) and cannabinol (CBN) as major putatively identified constituents based on relative peak area. The extract showed moderate free radical scavenging activity in a cell-free DPPH assay. Importantly, pre-treatment with the extract significantly reduced UVB-induced intracellular ROS accumulation. UVB exposure resulted in suppression of <i>MITF</i> mRNA expression, which was partially restored at higher extract concentrations, whereas transcript levels of <i>TYR</i>, <i>TYRP1</i>, and <i>TYRP2</i> remained largely unchanged under the experimental conditions. Functionally, the extract attenuated UVB-induced tyrosinase activity at the highest concentration tested, while total melanin content was not significantly altered.</p> Conclusions <p>Collectively, these findings suggest that a neutral cannabinoid-rich <i>C. sativa</i> extract (CSE) can mitigate UVB-induced oxidative stress and partially restore transcriptional regulation of <i>MITF</i> without inducing significant acute depigmentation. The extract may represent a candidate for further investigation as a bioactive component that may support skin cell homeostasis regarding its potential antioxidant-mediated photoprotective activity in dermatological formulations targeted at photo-oxidative stress.</p>

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Cannabis sativa L. extract modulates UVB-induced oxidative stress and MITF transcriptional suppression in B16-F10 melanoma cell line

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月1日

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  • Pakawadee Mahaprom,
  • Kannapat Narasuwan,
  • Natta Wiriyakun,
  • Piyanee Ratanachamnong,
  • Porntipa Korprasertthaworn,
  • Vasanop Vachiramon,
  • Pansakorn Tanratana

摘要

Background

Ultraviolet B (UVB) radiation disrupts skin homeostasis through reactive oxygen species (ROS)-mediated oxidative stress and melanogenic imbalance. The search for effective exogenous photoprotectants has highlighted natural products, including Cannabis sativa L. phytocannabinoids with reported antioxidant activity. However, their role in UVB-induced cellular responses remains to be clarified.

Methods

Chemical profiling was performed using LC-QTOF-MS and Fourier-transform infrared (FTIR) spectroscopy. Biological activities were assessed in B16-F10 pigmented melanoma cells, including cytotoxicity (MTT assay), intracellular ROS generation (DCFDA assay), transcriptional regulation of melanogenic markers (MITF, TYR, TYRP1, TYRP2) by RT-qPCR, and functional melanogenesis outcomes (tyrosinase activity and melanin content).

Results

LC-QTOF-MS revealed that the extract was dominated by neutral cannabinoids, with Δ⁹-tetrahydrocannabinol (Δ⁹-THC) and cannabinol (CBN) as major putatively identified constituents based on relative peak area. The extract showed moderate free radical scavenging activity in a cell-free DPPH assay. Importantly, pre-treatment with the extract significantly reduced UVB-induced intracellular ROS accumulation. UVB exposure resulted in suppression of MITF mRNA expression, which was partially restored at higher extract concentrations, whereas transcript levels of TYR, TYRP1, and TYRP2 remained largely unchanged under the experimental conditions. Functionally, the extract attenuated UVB-induced tyrosinase activity at the highest concentration tested, while total melanin content was not significantly altered.

Conclusions

Collectively, these findings suggest that a neutral cannabinoid-rich C. sativa extract (CSE) can mitigate UVB-induced oxidative stress and partially restore transcriptional regulation of MITF without inducing significant acute depigmentation. The extract may represent a candidate for further investigation as a bioactive component that may support skin cell homeostasis regarding its potential antioxidant-mediated photoprotective activity in dermatological formulations targeted at photo-oxidative stress.