Author et al | Animal type | Model | Intervention or component used to target Nrf2 signaling pathway | Outcomes |
---|---|---|---|---|
Chen et al. [107] | Mice | In vivo | Puerarin | • Increased follicle number and the primordial follicle ratio • Decreased the atresia ratio • Recovered the expression levels of Oct4, Mvh, Wnt1, β-catenin, cyclin D1, SOD2, and Nrf2 • Improved the Bcl-2/Bax ratio |
Chen et al. [109] | Rat | In vivo | Preventive Electroacupuncture | • Sex hormones recovered to normal levels • reducing OS in rats • Increasing SOD and GSH levels and decreased MDA levels • Dropping Keap1 protein expression • Increasing protein expressions of Nrf2 and HO-1 |
Ding et al. [99] | Mice | In vitro | EGF (epidermal growth factor) | • EGF suppressed OS by upregulating the expression of the NRF2/HO-1 pathway AND inhibited the apoptosis by regulating the PTEN/PI3K/AKT pathway |
Hu et al. [106] | Mice | In vivo | 4-Vinyl Cyclohexene Diepoxide | • 4-Vinyl Cyclohexene Diepoxide reduces OS damage in model of POI by upregulating Nrf2, Foxo3a, and HO-1 |
Jia et al. [101] | Mice | In vivo | Chitooligosaccharide-zinc | • Improves the ovarian and follicular development through regulating the SESN2/NRF2 signaling pathway • Elevates SOD2 protein |
Liu et al. [103] | Mice | In vivo | Sepia esculenta ink polysaccharide | • Reducing Keap1 and HDAC-2 • Increasing PKC, Nrf2 • Downstream factors like SOD, HO-1, and NQO-1 |
Chen et al. [105] | Mice | In vivo | Icariin | • Influenced POI by activating the Nrf2/HO-1/Sirt1 |
Yan et al. [98] | Mice | In vivo | Curcumin | • Inhibited D-gal-induced OS, apoptosis, and ovarian injury via a mechanism involving the Nrf2/HO-1 and PI3K/Akt signaling pathways in POI model |
Zhang et al. [108] | Mice | In vivo | Daphnetin (a Nrf2 activator) | • Alleviated POI through Nrf2/TXNIP/NLRP3 axis |
Zhou et al. [107] | Mice | In vivo | Si-Wu-Tang (a traditional Chinese medicine) | • Enhanced OS and promotes angiogenesis by targeting the Nrf2/HO-1 pathway in POI |