Alpha-mangostin attenuates the apoptotic pathway of abamectin in the fetal rats’ brain by targeting pro-oxidant stimulus, catecholaminergic neurotransmitters, and transcriptional regulation of reelin and nestin

Acetylated oligopeptide and N‐acetylcysteine protect against iron overload‐induced dentate gyrus hippocampal degeneration through upregulation of Nestin and Nrf2/HO‐1 and downregulation of MMP‐9/TIMP‐1 and GFAP

“…To the best of our knowledge, the effect of iron overload on nestin expression in the hippocampus has not previously been reported. It is believed that the iron overload‐induced oxidative stress led to disruptions in cell self‐regeneration responses 20 . This was significantly restored in both the NAC and AOP groups in comparison to the iron‐treated group.…”

“…Nestin is a class VI intermediate microfilament protein that is extensively expressed in neuronal precursor cells in the subventricular zone of the brain. It helps protect cells from a variety of stresses by regulating oxidative stress and, thus, maintaining intracellular redox homeostasis 20,21 . In addition, the oxidative damage that occurs after iron overload is thought to induce apoptosis, which in turn boosts neurodegeneration 22 .…”

“…It helps protect cells from a variety of stresses by regulating oxidative stress and, thus, maintaining intracellular redox homeostasis. 20,21 In addition, the oxidative damage that occurs after iron overload is thought to induce apoptosis, which in turn boosts neurodegeneration. 22 Members of the caspase family are proteolytic enzymes that induce apoptosis via extrinsic and intrinsic apoptotic pathways.…”

Ginger reserves testicular spermatogenesis and steroidogenesis in difenoconazole‐intoxicated rats by conducting oxidative stress, apoptosis and proliferation

“…2020). This complex can initiate caspase‐9 activation that, consequently, prompts the transcriptional activation of caspase‐3 which triggers apoptosis (Ibrahim et al., 2021) and DNA fragmentation. As the spermatogonia and early dividing spermatocytes are the primary susceptible testicular cells to apoptosis (Eggert et al., 2019), the increased activity of Ki‐67 in the seminiferous tubule after difenoconazole exposure was mostly in spermatogonia and primary spermatocytes as adaptive feedback to protect the testicular cells against apoptosis.…”