Tag Archives: reactive oxygen species

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

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A cannabinoid-rich Cannabis sativa extract reduced UVB-induced oxidative stress in B16-F10 melanoma cells used to study pigmentation responses. Pretreatment lowered the buildup of reactive oxygen species—molecules that can damage cells when produced in excess. Chemical profiling tentatively identified THC and cannabinol (CBN) as major extract constituents.

UVB exposure suppressed expression of MITF, a regulator involved in pigment production, and higher extract concentrations partially restored it. At the highest concentration tested, the extract also reduced UVB-induced activity of tyrosinase, an enzyme involved in making pigment. Total melanin content, however, did not change significantly.

These findings support further investigation of cannabis-derived compounds for formulations targeting UV-related oxidative stress and cellular balance.

“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.”

https://pubmed.ncbi.nlm.nih.gov/42947120

“In conclusion, this study establishes that an ethanolic CSE, characterized by a lipophilic terpene-phenolic matrix of neutral cannabinoids, serves as a potential cytoprotective modulator against UVB-induced oxidative injury. Our data demonstrates that CSE effectively neutralizes intracellular ROS accumulation and partially restores the transcriptional suppression of MITF.

By bridging chemical profiling with molecular resilience, these results provide a strong mechanistic roadmap for utilizing cannabis-derived extracts to enhance skin homeostasis against solar radiation, offering a strong foundation for verifying its full photoprotective capacity in future models.”

https://link.springer.com/article/10.1186/s12906-026-05487-z

Cannabinoids in Cancer: Molecular Mechanisms of Tumor Cell Death and Translational Opportunities

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Cannabinoids can attack cancer cells through far more than a single mechanism. This 2026 review describes how natural and synthetic cannabinoids can suppress tumor-cell growth, angiogenesis and metastasis while activating multiple forms of regulated cancer-cell death, including apoptosis, autophagy-dependent cell death, necroptosis, ferroptosis and parthanatos.

The researchers detail an interconnected network of molecular pathways affected by cannabinoids, including PI3K/AKT/mTOR, MAPK/ERK, NF-κB, TRIB3/AKT/mTORC1 and ceramide/ROS signaling. These pathways control whether cancer cells survive, proliferate, respond to stress or undergo programmed destruction, giving cannabinoids multiple potential points of attack against malignant cells.

The review also finds that cannabinoids may enhance conventional anticancer treatments by engaging complementary cell-death pathways. The authors conclude that cannabinoids represent promising anticancer agents and therapeutic adjuvants, with much of the direct anticancer evidence still coming from preclinical research and clinical translation now depending on better dosing, formulations and controlled human studies.

“Cannabinoids are terpenophenolic compounds derived from Cannabis sativa L. that exert a broad range of biological and pharmacological activities. Increasing evidence highlights their potential as modulators of cancer progression specifically through the suppression of tumor cell growth, angiogenesis, and metastasis across multiple tumor models.

This review provides a comprehensive overview of the molecular mechanisms by which natural and synthetic cannabinoids induce regulated cancer cell death.

Current evidence demonstrates that cannabinoids regulate multiple forms of cancer cell death, including apoptosis, autophagy-dependent cell death, necroptosis, ferroptosis, and parthanatos. These effects are mediated through complex and interconnected signaling pathways such as TRIB3/AKT/mTORC1, PI3K/AKT/mTOR, MAPK/ERK, NF-κB, ERK/JNK/p38-MAPK, and ceramide/Raf1/ERK/ROS.

In addition to their direct antitumor effects, cannabinoids can enhance the efficacy of conventional anticancer therapies through the coordinated regulation of complementary cell death pathways. They also provide clinically relevant supportive benefits in palliative care, alleviating chemotherapy-induced nausea, cachexia, and mood or sleep disturbances.

Collectively, these findings identify cannabinoids as promising anticancer agents and therapeutic adjuvants, predominantly in the preclinical setting. However, significant challenges remain regarding their safety, optimal dosing, formulation, and clinical efficacy. Further mechanistic studies, rigorous preclinical research, and well-designed clinical trials are required to establish the translation of cannabinoid-based therapies into precision oncology.”

https://pubmed.ncbi.nlm.nih.gov/42793092

“The cannabis plant, a member of the Cannabaceae family, has been traditionally utilized for centuries for spiritual and remedial healing.”

“The anticancer activity of cannabinoids was discovered in 1975 by Munson et al.. Cannabinoids suppress cancer cell proliferation, angiogenesis, tumor invasion, metastasis, and stemness while inducing different modes of cell death pathways.”

“In summary, this review highlights the growing body of evidence supporting the ability of cannabinoids to induce multiple forms of cell death across a broad spectrum of cancer types. Through the modulation of diverse molecular and signaling pathways, cannabinoids have emerged as promising anticancer agents, mostly in preclinical models, with the potential to target tumor growth, survival, and progression, ultimately triggering diverse cell death mechanisms.”

https://www.mdpi.com/2218-273X/16/9/1260