Ebru Bardaş Özkan

The study tests the efficacy of subconjunctival ranibizumab and bevacizumab treatments in determining the oxidant and antioxidant levels during alkali-induced corneal neovascularisation. The researchers assigned 24 New Zealand White rabbits into four different groups, which included a healthy control, an alkali-injured control, a BV-treated group, and an RN-treated group, with six rabbits per group. All animals received alkali injury treatment except for the HC group. The AC group received six doses of subconjunctival saline 24 h after their injury, while the BV group and RN group received one dose of 0.5 mg of their respective treatment. The researchers conducted 14-day assays on normal tissue, blood plasma, and erythrocytes to determine total antioxidant status and total oxidant status. The researchers performed biochemical assays for total antioxidant status TAS and total oxidant status TOS on samples that were collected after the 14-day observation period. The corneal TOS levels increased in all injured groups when matched against the HC group. The RN group showed the highest corneal TOS levels, but the difference between the RN and AC and BV groups did not reach statistical significance. The injured groups showed higher corneal TAS levels than HC (p = 0.002), but the AC, BV, and RN groups showed no differences. The injured groups showed a significant decrease in erythrocyte TAS compared with HC (p < 0.001), but the injured groups showed lower plasma TOS levels than HC (p < 0.001). The researchers found no other systemic differences between the groups that received anti-VEGF treatment. The study results show that alkali injury leads to both local and systemic changes in redox status. The two anti-VEGF agents caused numerical changes in corneal oxidative parameters, but these changes did not achieve statistical significance. The research requires further investigation to understand potential agent-related effects on corneal redox balance, which should take place in larger, more detailed studies.

In brain ischaemia (BI), the oxidative and ionic stresses lead slowly but definitely to the injury of neurones. The present investigation is looking to check the status of certain oxidative stress markers and trace elements which are induced in response to brain ischaemia with sodium valproate (VPA), a neuroprotective agent, in the rats exposed to the model of BI. Although VPA is already used for clinical purposes, it deserves careful examination of the potentially detrimental effects of VPA in conditions of ischaemia closely linked to hepatotoxicity and thrombocytopenia. Forty rats were randomly assigned into five groups (n = 8 per group): Control, Sham, Brain Ischaemia (BI), BI + Valproic Acid (VPA), and VPA only. Ischaemia was induced in the BI and BI + VPA groups by bilateral occlusion of the common carotid arteries for 30 min. VPA was administered orally at a dose of 100 mg/kg daily for seven days in the BI + VPA and VPA-only groups. This dose was based on previous preclinical safety and efficacy data. Control, Sham, and BI groups received saline. The Sham group underwent surgical procedures without carotid occlusion. The biochemical investigations pertaining to cortical tissue demonstrated the fact that BI has decreased all antioxidant enzyme levels of SOD, CAT, GPx, and those of trace elements such as Mg, Zn, and Se. At the same time, malondialdehyde (MDA) and neurotoxic metals (Cr, Fe, Cu) increased. These changes brought by BI were restored through treatment with VPA on oxidative stress and the restoration of trace element balance along with reductions in those associated with oxidative damage. The results thus reinforce the capacity of VPA for neuroprotective benefits against ischaemic damage inflicted within brain tissue and hence merit the further exploration of the mechanistic action of this therapeutic A.