Table 1 The role of Nrf2 in ovary
Author et al | Animal type | Model | Component used to target Nrf2 signaling pathway | Outcomes |
|---|---|---|---|---|
Zheng et al. [58] | zebrafish | In vivo | Cadmium | • Activated key transcription factors, Nrf2 and NF-kB • Increase Tumor Necrosis Factor-alpha (TNF-α) |
Fan et al. [59] | Rat | In vivo | Atrazine | • Improved the oocyte maturation • Increased mRNA abundance of NRF2, SOD1, CAT, and GPX4 |
Xue et al. [60] | Mice | In vivo | Carbon tetrachloride | • Antioxidants such as SOD, NRF2, and HO-1 were decreased • Inflammation markers were increased |
Ma et al. [61] | Laying Hens | In vivo | Mercury (Hg) | • Disrupted oocyte maturation through decreasing Nrf2-Cyclin B1 signaling pathway |
Xu et al. [62] | Mice | In vivo | Zinc Oxide particle | • Upregulation of antioxidant-related genes, ER stress-related genes and genes related to apoptosis • increased atretic follicles and exfoliated follicular granulosa cells |
Grzegorzewska et al. [63] | Chicken Embryonic Gonads | In vitro | Sodium florid | • disrupt normal antioxidant balance in developing reproductive organs • increase the intensity of immunolocalised antioxidant markers like CAT, SOD2, and Nrf1 in the ovary |
Ma et al. [64] | Hens | In vivo | vanadium + epigallocatechin-3-gallate | • Vanadium exposure reduced antioxidant enzymes (SOD, CAT, GR, GSH-Px), but EGCG supplementation restored these enzyme activities • EGCG has ability to enhance Nrf2 and sMaf gene expression |
Shain et al. [65] | Japanese quail | In vivo | Capsaicinoids supplement against heat stress | Heat Stress effects • Increases OS markers • Decrease levels of Nrf2, Akt, and HO-1 Capsaicinoids effects • Increase antioxidant markers Nrf2, Akt, and HO-1 |
Xing et al. [66] | Hens | In vivo | Resveratrol | • lower inflammation markers promotes antioxidant signaling pathways |
Meng et al. [67] | Rat | In vivo | Co-administration Hydrogen-rich saline with Cisplatin | • improved ovarian function by reducing markers like MDA and increasing protective antioxidants SOD, CAT • elevated estrogen (E2) levels, reduced FSH |
Niringiyumukiza et al. [68] | Mic | In vivo | Co-administration glycogen synthase kinase-3 inhibition with Doxorubicin | • increase the expression of Nrf2 and restored GSH-Px and SOD-1 levels • supporting ovarian recovery by restored AMH and E2 levels and lowered FSH |
Sun et al. [69] | Rat | In vitro | Melatonin | • activation of antioxidative enzymes via the Nrf2 signaling Pathway • scavenge ROS |
Guo et al. [50] | Mic | In vitro | Melatonin | • melatonin regulates the expression of genes Nrf2, SOD1 and proteins Nrf2, HO-1 • Mitigating intracellular OS, consequently enhancing in vitro development of vitrified-warme germinal vesicle oocytes |
Raghuraman et al. [48] | Chinese Hamster Ovary (CHO) cells and murine splenic lymphocytes | In vitro | Diselenonicotinamide (DSNA), 1.26 | •. Increase antioxidant activity • Reduce radiation-induced DNA damage • Upregulation of repair gene RAD51 |
Sze et al. [52] | Rat | In vitro, in vivo | Aging and iron metabolism | • Nrf2 Downregulation • elevated expression of ovarian inflammatory factors such as (iNOS and TNFα) via NF-κB activation • iron accumulation and ferroptosis |
Akino et al. [53] | Mic | In vivo | Dimethylfumarate 20 mg/kg, oral | • increase Nrf2 and antioxidant levels • reduce DNA damage, and OS in the ovary |
Lim et al. [55] | Mic | In vitro | • deletion of Nrf2 and benzo [a] pyrene | • depletion of ovarian follicles in both Nrf2 + / + and Nrf2 − / − mic • ovarian aging accelerates in the absence of NRF2 |
Bai et al. [54] | Mic | In vivo | Tanshinone IIA | • enhances the ovarian reserve and attenuates ovarian OS |
Tsakiri et al. [56] | Drosophila melanogaster | In vivo, in vitro | proteasome | • Unlike gonads, proteasome expression and activity decline in aged somatic tissues • age-related Nrf2 dysfunction is correlated with the diminished levels of proteasomes |
Li et al. [57] | Mic | In vivo | Deletion of pigment epithelium-derived factor | • Increased the level of ROS and activated the Nrf2 pathway • Decrease ovarian reserve |
Gong et al. [70] | CHO cells (Ka13) | In vitro | cobalt chloride and hypoxia | • CoCl2 ctivates Ho-1gen through OS and the involvement of Nrf2 and MafG • Hypoxia uses a distinct pathway without involving these proteins for Ho-1gen exprssion |
He et al. [71] | CHOK1SV cells | In vitro | Altering the medium cell cultures | • reduce oxidation of monoclonal antibodies (mAbs), specifically tryptophan oxidation • reduce ROS through the Nrf2-mediated antioxidative response |