Abstract ▼ AI-Helper

Oxidative stress induces cellular senescence and causes various diseases such as age-related macular degeneration or ischemic diseases. Oxidative stress is caused by various endogenous and exogenous stresses, among which free radicals such as ROS are the main causes of oxidative stress. ROS is induc...

Oxidative stress induces cellular senescence and causes various diseases such as age-related macular degeneration or ischemic diseases. Oxidative stress is caused by various endogenous and exogenous stresses, among which free radicals such as ROS are the main causes of oxidative stress. ROS is induced by a variety of stimuli, primarily at the site of formation, with a short half-life and high reactivity. Pre-oxidants such as ROS are involved in the cellular redox system to maintain normal cellular metabolism if they are in proper amounts, but they can cause oxidative stress while causing an imbalance when they are more abundant than antioxidants. Therefore, we induced oxidative stress by inducing ROS using H2O2. First, gold nanoparticles (GNPs) was synthesized and analyzed using biologically active natural substances as a reducing agent, and GJ-GNPs and antioxidant lutein, were used for antioxidant and anti-senescence in retinal pigment epithelium to confirm the efficacy. Therefore, the contents of lysosome, ROS, and SA--gal were analyzed to confirm the decrease of the increased contents in the senescent cells. Cell cycle recovery was also observed, through changes and increases in protein expression associated with antioxidant and anti-senescence (HO-1, NQO1, SIRT1, SIRT3) and showed cell protection system in oxidative stress and cellular senescence. It appears to be available in the treatment of retinal-related diseases such as age-related macular degeneration (AMD) and in regenerative medicine.
Oxidative stress and cellular senescence also lead to cellular damage and DNA damage and abnormalities in the mitochondria, followed tissue injury. In addition, there is a high generation of ROS in that part of the tissue transplant, which can lead to oxidative stress. Here, we exploited bioinspired phage nanofibers, previously recognized by its biochemical and structural cues inducing angiogenesis, as an antioxidant tissue engineering material. In this study, we tried to identify the potential for tissue regeneration via using antioxidant efficacy using engineered M13 bacteriophages as tissue engineering materials. We induced oxidative stress using H2O2 in HUVECs and HeLa cells, and confirmed the antioxidant potential through cell viability, morphological observation, and changes in the contents of lysosome, ROS, and SA--gal. Activation of the ERK/Nrf2 signaling pathway by R8 bacteriophage led to Nrf2 to the nucleus translocation, and induction of the expression of antioxidant genes such as HO-1 and NQO1. These antioxidant factors show anti-oxidative effect and seem to protect against oxidative stress. In addition, angiogenesis due to the presence of RGD, which has superior cell attachment ability, is shown to be due to the JNK signaling pathway. Thus, we have developed nanomaterials and nano carriers that have antioxidant and anti-senescence properties against oxidative stress and cellular senescence, and they appear to play an important role in protecting cells against oxidative stress and senescence, in particular GJ-GNPs can be a new therapeutic strategy for age-related macular degeneration and retina-related regenerative medicine. Also, this vascular and antioxidant niche providing bioinspired phage nanofibers can serve novel therapeutic platform for curing ischemic diseases, or it can be used in the field of tissue regeneration and engineering.

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