Table 1.
Biological effects | Main mechanisms | References |
---|---|---|
Anti-inflammation |
Inhibits IL-1β, IL-6, TNF-α, HMGB-1, ICAM-1; Inhibits M1 polarization, increases M2 polarization of macrophages; Inhibits the recruitment of neutrophils to lesion sites, inhibits adhesion of polymorphonuclear neutrophils to ECs; The involved pathways: NF-κB, NLRP3, TLR4, Nrf2 |
Buchholz et al. (2008), Kawamura et al. (2013), Xiao et al. (2013), Ren et al. (2014), Chen et al. (2015b), Liu et al. (2015a), Shi et al. (2015), Xie et al. (2015), Zhai et al. (2015), Tian et al. (2017), Ning et al. (2018), Yu et al. (2019), Zou et al. (2019), Ming et al. (2020), Yang et al. (2020), Qiu et al. (2021) |
Anti-oxidation |
Directly scavenges ·OH and ONOO−; activates Nrf-2/ HO-1; upregulates the expression of SOD, CAT, GSH-Px, downregulates NADPH oxidase; hormesis through increasing ROS |
Ohsawa et al. (2007), Yu and Zheng (2012), Shinbo et al. (2013), Hirayama et al. (2018), Zhao et al. (2019) |
Modulates autophagy | Promotes autophagy when autophagy is insufficient; inhibits autophagy when excessive autophagy disrupts cell homeostasis | Zhang et al. (2015), Yao et al. (2019), Chen et al. (2020a), Zhuang et al. (2020), Qiu et al. (2021) |
Modulates cell death |
Antiapoptosis: inhibiting Bax, caspase-3, and caspase-8, upregulating Bcl-xl and Bcl-2 Inhibits pyroptosis by inhibiting oxidative stress, NLRP3 and mitoKATP/ERK1/2/p38 MAPK signaling pathways |
Cai et al. (2008), Kawamura et al. (2010), Du et al. (2016), Nie et al. (2021), Zhang et al. (2021) |