Activation of cerebral peroxisome proliferator-activated receptors gamma exerts neuroprotection by inhibiting oxidative stress following pilocarpine-induced status epilepticus

Dietary low or excess levels of lipids reduced growth performance, and impaired immune function and structure of head kidney, spleen and skin in young grass carp (Ctenopharyngodon idella) under the infection of Aeromonas hydrophila

“…Second, lipids may increase the GSH content and induce ROS production in the skin of young grass carp. Studies have reported that lipids were able to activate PPARg in mammals [34], and up-regulated PPARg protein levels could increase GSH content in the rat brains [35]. In our research, excess lipids could induce ROS production in the skin of young grass carp.…”

“…Studies report that dietary supplementation with lipids could enhance the activities of catalase (CAT) in the mouse liver [33]. Additionally, it was reported that lipids were able to activate peroxisome proliferator-activated receptor gamma (PPARg) in mammals [34], and up-regulated PPARg protein levels could increase the GSH content and activate Nrf2 gene expression in the rat brain and H4IIE cells, respectively [35]. Furthermore, Carratelli et al [36] reported that lipids supplementation could up-regulate the protein levels of 70-kDa heat shock protein (hsp70) in mouse splenic lymphocytes.…”

Ketogenic diets, mitochondria, and neurological diseases

“…In contrast, FMOC-Lleucine did not exhibit anti-seizure activity in another seizure model, the 6 Hz test, and another PPAR ␥ ligand, rosiglitazone, did not reduce audiogenic seizures ( 133 ). Rosiglitazone has been shown to reduce oxidative stress in the lithium-pilocarpine model of epilepsy, and this was associated with an amelioration of neuronal death in the hippocampus and an enhancement of superoxide dismutase (SOD) activity and levels of GSH, as well as a reduction in the Nrf2 target, heme oxygenase-1 ( 134 ). Further, the PPAR ␣ -selective agonist ciprofi brate was shown to selectively increase mRNA levels of HMG-CoAS2, the ratelimiting enzyme in the production of ketone bodies, and that of two other known PPAR ␣ targets, acyl CoA oxidase and medium-chain acyl-CoA dehydrogenase ( 135 ).…”

The Impact of Fish Oil on the Chemopreventive Efficacy of Tamoxifen against Development ofN-Methyl-N-Nitrosourea–Induced Rat Mammary Carcinogenesis

“…Because PPARγ activation is known to inhibit oxidative stress (12,13), which, in turn, can affect carcinogenesis (14-16), we examined the effects of our treatments on circulating and tumor GSH levels as indicators of the level of oxidative stress. As can be seen in Table 4, a significant increase in red blood cell levels of both free and protein-bound GSH was observed in all groups of rats injected with MNU compared with rats not given the carc i n o g e n .…”

“…Although estrogen receptor activation has been shown to suppress PPARγ-mediated transcription, estrogen receptor antagonists such as ICI182780 and 4-hydroxy-tamoxifen have been shown to stimulate PPARγ transactivation and to potentiate the antiproliferative activity of a PPARγ agonist in breast cancer cells (10). Activation of PPARγ has recently been shown to inhibit oxidative stress (12,13), thus raising the possibility that this could be a mechanism of cooperativity between tamoxifen and n-3 PUFA in suppressing mammary carcinogenesis. Modification of oxidative stress has indeed been proposed as one of the mechanisms by which n-3 PUFA exert their antitumor action (14)(15)(16).…”