Inhibition of acrolein-induced autophagy and apoptosis by a glycosaminoglycan from Sepia esculenta ink in mouse Leydig cells

The effect of melanin-free extract from Sepia esculenta ink on lipid peroxidation, protein oxidation and water-holding capacity of tilapia fillet during cold storage

“…Secondly, SIP activated Nrf2/ARE pathway, an important antioxidation-associated signaling pathway, to delete oxidants [ 24 ]. Thirdly, SIP can prevent effectively cells from oxidants induced autophagy, ameliorating formation of autophagosome [ 15 , 25 ]. Therefore, in our current research, a possible mechanism was that the liberation of hydrolases from lysosomes was inhibited by SIP, so that the degradation of protein and the formation of TVBN were weakened.…”

ERO1α promotes testosterone secretion in hCG‐stimulated mouse Leydig cells via activation of the PI3K/AKT/mTOR signaling pathway

“…The PI3K/AKT/mTOR signaling pathway plays an important role in Leydig cells proliferation, survival, and apoptosis (Ding, Wang, Li, & Ma, 2016; Gu et al, 2017; Pan, Wang, Lai, Mu, & Huang, 2015; Park, Park, Lim, & Song, 2019; J. H. Sun et al, 2017; Yang et al, 2019; H. Zhang et al, 2019; P. H. Zhou, Hu, Zhang, Wang, & Zhang, 2016). PI3K catalyzes the phosphorylation of AKT and activates downstream the mTOR signaling pathway subsequently mediates phosphorylation of P70S6K to initiation of protein translation.…”

“…The PI3K/AKT/mTOR signaling pathway plays an important role in Leydig cells proliferation, survival, and apoptosis (Ding, Wang, Li, & Ma, 2016;Gu et al, 2017;Pan, Wang, Lai, Mu, & Huang, 2015;Park, Park, Lim, & Song, 2019;J. H. Sun et al, 2017;Yang et al, 2019;P.…”

A Potential Adjuvant Agent of Chemotherapy: Sepia Ink Polysaccharides

“…SIP has been verified to have chemoprophylactic actions on the reproductive system [ 29 , 48 , 49 , 50 , 51 , 52 , 53 ]. When male mice exposed to cyclophosphamide were administered SIP, the abnormal rates of their sperm declined, and the foetal abnormalities in female mice mated with them also declined, with total foetal count and average foetal count increasing [ 48 ].…”

“…In addition, SIP can prevent animals from cyclophosphamide-mediated mutation in vivo and H 2 O 2 /UV-induced DNA strand break in vitro [ 28 , 65 ]. The testicular cells of cyclophosphamide-exposed mice, including spermatogonia, Sertoli cells, and Leydig cells, were protected by SIP via repression of cyclophosphamide-induced autophagy-associated cell death and apoptosis; the mechanisms involved p38 mitogen-activated protein kinase and phosphoinositide 3-kinase PI3K)/Akt signalling pathways [ 51 , 52 , 53 ]. Similarly, for cyclophosphamide-mediated ovarian failure, SIP also successfully inhibited follicle deletion and granule cell disruption by repressing cyclophosphamide-induced autophagy-associated cell death and apoptosis via regulation of p38 mitogen-activated protein kinase and PI3K/Akt pathways, resulting in functional rescue of the ovaries of cyclophosphamide-exposed mice [ 29 ].…”