We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Protective role of SIRT1 activation against retinal injury caused by polystyrene micro/nanoplastics exposure
Summary
Tiny plastic particles (the kind found widely in our environment) can build up in eye tissue and damage cells in the retina, the part of your eye responsible for vision, by increasing harmful oxidative stress and speeding up cell aging. Researchers found that boosting a protective protein called SIRT1 with a drug-like activator helped shield retinal cells from this plastic-induced damage in both lab-grown cells and rats. While more research is needed before this becomes a treatment for humans, the study suggests a promising target for protecting eye health as microplastic pollution continues to rise.
Plastic particles are persistent environmental pollutants that can accumulate in ocular tissues and potentially contribute to retinal damage. Sirtuin 1 (SIRT1), a key regulator of oxidative stress and cellular senescence, may play a protective role against plastic-induced retinal injury, but its role remains unclear. In this study, human retinal pigment epithelial (RPE) cells and rat retinas were directly exposed to polystyrene microplastics (PS-MPs, 2 μm) and nanoplastics (PS-NPs, 50 nm), with and without SIRT activator SRT1720. In vitro analyses included cell viability, intracellular reactive oxygen species (ROS), SIRT1 expression, antioxidant enzyme levels (SOD1, SOD2, CAT), and senescence were assessed. In vivo, rats received intravitreal injections of plastic particles, with or without SRT1720 and oxidative stress-related markers, SIRT1 expression, and senescence were evaluated in retinal tissues 7 days after injection. Results showed that PS-MPs and PS-NPs reduced RPE cell viability in a dose- and time-dependent manner, suppressed SIRT1 and antioxidant enzymes, and increased ROS and senescence. PS-NPs induced stronger ROS and senescence than PS-MPs in vitro. Co-treatment with SRT1720 restored SIRT1 expression, improved antioxidant responses, and attenuated ROS and senescence. In vivo, both particle types induced retinal changes similar to those observed in cell experiments. However, there was no significant toxicity difference between PS-MPs and PS-NPs. In conclusion, PS-MPs or PS-NPs promote oxidative stress and senescence in RPE cells and retinal tissue via downregulation of SIRT1 and antioxidant defenses, while SRT1720 provides protective effects. These findings SIRT1 as a potential therapeutic target for plastic-induced retinal injury.