Rabbit Anti-Human SOD2 Polyclonal Antibody

Berberine (BBR), an isoquinoline alkaloid, has been reported to be an antioxidant agent. This study was conducted to investigate the effect of BBR against nephrotoxicity induced by cisplatin (Cis) in male rats. In this experimental study, 28 Wistar male rats were randomly divided into four groups. Rats were pretreated with BBR (100 mg/kg/day, p.o.) for 7 consecutive days and Cis (7.5 mg/kg, i.p.) was administrated on the 7th day, 1 h after the last dose of BBR. Blood samples were collected to determine blood urea nitrogen (BUN) and creatinine (Cr) levels. Malondialdehyde (MDA), glutathione (GSH), protein carbonyl (PC), and nitric oxide (NO) levels and the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and myeloperoxidase (MPO) were assessed in the left renal tissue. Also, the mRNA expression of SOD2 and PGx1 was measured in the left renal tissue. The right kidney was used for histopathological evaluation. Our results revealed that the levels of Cr, BUN, MDA, NO, and PC and the MPO activity increased by Cis administration. Also, we found that Cis decreased renal GSH level and SOD, GPx, and CAT activities. Pretreatment with BBR for 7 consecutive days significantly attenuated the Cis-induced nephrotoxicity via increasing the antioxidant capacity and reducing the oxidative stress indices in the renal tissue. Moreover, the renoprotective effect of BBR was confirmed by the histopathological evaluation of the kidneys. Our results indicated that BBR has produced amelioration in biochemical indices and oxidative stress parameters against Cis-induced nephrotoxicity.

Oxidative stress has been associated with the etipathogenesis of Diabetic retinopathy (DR). Studies have shown that DJ-1 plays an important role in regulating the reactive oxygen species (ROS) production and resistance to oxidative stress-induced apoptosis. This study aimed to investigate whether DJ-1 upregulates oxidative stress and prevents damage to retinal capillary pericytes by increasing antioxidant capacity through the Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. Nrf2 is a redox-sensitive transcription factor that encode antioxidant enzymes and phase II metabolic enzymes, activation of Nrf2 functions is one of the critical defensive mechanisms against oxidative stress in many tissues. Our results showed after DJ-1 overexpression, apoptosis of rat retinal pericytes (RRPs) decreased, the ratio of B-cell lymphoma-2 (Bcl-2) to BCL2-Associated X Protein (BAX) increased, the production of ROS decreased, and the protein expression and activity of manganese superoxide dismutase (MnSOD, also called SOD2) and catalase (CAT) increased. DJ-1 overexpression activated Nrf2 expression, however, after Nrf2 silencing, apoptosis of RRPs increased, the ratio of Bcl-2 to BAX decreased, the production of ROS increased, the protein expression of MnSOD and CAT decreased, and the expression of heme oxygenase-1 (HO-1), NADP(H) quinone oxidoreductase (NQO1), glutamate-cysteine ligase catalytic subunit (GCLC) and modifier subunit (GCLM) decreased. These data suggest that enhancement of the Nrf2 pathway is a potential protective strategy for the treatment of DR. Therefore, DJ-1 may prevent high glucose-induced oxidative stress and RRPs apoptosis through the Nrf2 signaling pathway, thereby preventing the early onset and progression of DR.