| Resveratrol |
Increases mitochondrial mass and mitochondrial DNA. Activates SIRT1 and upregulates NO and eNOS. Activates Nrf2 pathways. |
Avotri, Eatman & Russell-Randall (2019), Coralia et al. (2011)
|
| Lycium barbarum polysaccharides (LBP) |
Activates the PI3K/AKT and ERK signaling pathways by upregulating miR-4295. |
Liu & Zhang (2019) |
| Curcumin |
Inhibits proinflammatory factors, including IL-6, ELAM-1, IL-1α, and IL-8, decreases the activities of the senescence marker SA-β-gal, and lowers the levels of carbonylated proteins and the number of apoptotic cells. |
Lin, Ciolino & Pasquale (2017) |
| Baicalin |
Increases cell survival and decreases iROS production. Inhibits the production of IL-1α and ELAM-1, decreases the activity of senescence-associated SA-β-gal, and lowers the level of carbonylated proteins. |
Gong & Zhu (2018) |
| Sulforaphane |
Attenuates H2O2-induced oxidative stress via PI3K/AKT-mediated NRF2 signaling activation. |
Liu & Zhang (2019) |
| Quercetin |
Upregulates antioxidant peroxiredoxins through the activation of the NRF2/NRF1 transcription pathway and protects against oxidative stress-induced ocular disease. |
Naoya et al. (2011) |
| Procyanidins |
Decreases the apoptotic rate of TMCs under oxidative stress and reduces the release of cytochrome C. |
Shi & Wang (2017) |
| Salidroside |
Protects TMCs against H2O2-induced oxidative damage by activating the PI3K/AKT and Wnt/β-catenin pathways by increasing miR-27a. |
Zhao et al. (2019a), Zhao et al. (2019b)
|
| Polyphenols (derived from red wine, tea and dark chocolate) |
Targets eNOS and induces the accumulation of NRF2. |
Mann et al. (2007), Upadhyay & Dixit (2015)
|
| Rapamycin |
Protects TM-1 cells from COS by inhibiting mTOR and inducing autophagy. In addition, removes damaged mitochondria. |
He et al. (2019) |
| Ethyl pyruvate |
Able to nonenzymatically reduce hydrogen peroxide and scavenge hydroxyl radicals. |
Dobsak et al. (1999), Famili, Ammar & Kahook (2013)
|
| 1α,25-dihydroxyvitamin D3 |
Attenuates OS-induced damage in TMCs by inhibiting TGFβ-SMAD3-VDR pathway |
Lv et al. (2019) |