Recent studies have highlighted the protective benefits of traditional Chinese medicinal plants, with Abelmoschus manihot (L.) medic flowers (TEA) showing promising results against oxidative stress. This research explores how TEA can shield human skin cells (HaCaT cells) from the detrimental effects of harmful substances like hydrogen peroxide (H2O2), which is known to induce oxidative damage and cell death.
The skin, as the body’s primary barrier, is frequently exposed to environmental pollutants, ultraviolet rays, and various hazardous compounds, leading to increased rates of skin diseases linked to oxidative stress. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify these harmful components. Accumulated ROS can aggravate tissue damage, particularly within the skin, resulting in scarring and inflammatory responses.
This study has found TEA to exert potent antioxidant effects, confirming its traditional use for skin-related ailments. By simulating oxidative stress conditions with H2O2, researchers observed how TEA not only improved cell viability but also reduced apoptosis, showcasing its capacity to protect HaCaT cells from oxidative damage.
Utilizing various techniques, including MTT assays and membrane potential assessments, the researchers discovered significant changes post-TEA treatment. Specifically, TEA administration led to decreased levels of intracellular ROS and malondialdehyde (MDA), along with increased superoxide dismutase (SOD) activity, which is integral to the antioxidant defense mechanism.
Further investigations revealed the interplay between TEA and the kelch-like ECH-associated protein 1 (KEAP1)/nuclear factor E2-related factor 2 (Nrf2) signaling pathway. Under normal conditions, Nrf2 remains inactive within the cytoplasm. This study demonstrated how H2O2 exposure resulted in the liberation of Nrf2 from KEAP1, permitting its movement to the nucleus where it can initiate the expression of antioxidant proteins. TEA was shown to amplify this process, enhancing the expression levels of Nrf2 and its downstream targets like NAD(P)H:quinone oxidoreductase 1 (NQO1), thereby mitigating oxidative stress.
Central to the findings is the mitochondrial transcription factor A (TFAM), whose roles include mitochondrial DNA replication and transcription, directly influencing mitochondrial function. The connection between Nrf2 and TFAM was established, with the data indicating TEA’s protective role extends beyond immediate antioxidant activity. Knockdown experiments demonstrated TEA's reliance on the Nrf2/TFAM axis for its protective effects against H2O2-induced damage.
TEA treatment also positively impacted mitochondrial morphology, preserving membrane potential and function, which is often compromised during oxidative stress. After treatment, mitochondrial ATP levels and mtDNA copy number improved significantly, indicating enhanced mitochondrial biogenesis and function. Collectively, these results elucidate TEA’s underlying mechanisms through which it combats oxidative stress, proposing its clinical potential for preventing skin damage caused by environmental stressors.
Research findings affirm the traditional use of TEA as not merely folkloric wisdom but as scientifically substantiated therapy. Future studies could explore its applications beyond dermatology, potentially aiding various oxidative stress-related conditions. The clear link between natural remedies, such as TEA, and modern scientific understandings of cellular protection may pave the way for new therapeutic strategies bolstered by traditional medicine.