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The purpose of this study was to evaluate the effects of syringic acid, an anti-oxidant, on indomethacin induced gastric ulcers in rats. Experimental groups were control, ulcer, ulcer treated with 20 mg/kg esomeprazole (a proton pump inhibitor that reduces acid secretion), and ulcer treated with 100 mg/kg syringic acid. Rats were pretreated with esomeprazole or syringic acid two weeks before ulcer induction. Our histopathological observations showed that either syringic acid or esomeprazole attenuated the severity of gastric mucosal damage. Moreover, syringic acid and esomeprazole pretreatments alleviated indomethacin-induced damage by regulating oxidative stress, inflammatory response, the level of transforming growth factor-β (TGF-β), expressions of COX and prostaglandin E2, cell proliferation, apoptosis and regulation of the NF-κB signaling pathway. We conclude that either esomeprazole or syringic acid administration protected the gastric mucosa from harmful effects of indomethacin. Syringic acid might, therefore be a potential therapeutic agent for preventing and treating indomethacin-induced gastric damage. [ABSTRACT FROM AUTHOR]

Objective: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons, leading to motor impairments and cognitive deficits. Despite advances in understanding PD's pathophysiology, effective therapeutic interventions are limited. Oxidative stress, resulting from the overproduction of reactive oxygen and nitrogen species, plays a crucial role in PD progression. Neurosteroids, naturally occurring brain steroids, have been implicated in dopamine signaling regulation and are disrupted in PD. Pregnenolone (Prgn), a neurosteroid, has shown potential neuroprotective properties and antioxidant effects. Methods: In this study, we investigated the neuroprotective potential of Prgn in an in vitro PD model using SH-SY5Y cells treated with 6-hydroxydopamine (6-OHDA). Pregnenolone pretreatment significantly improved cell viability and reduced oxidative stress induced by 6-OHDA exposure. Moreover, Prgn treatment led to the modulation of antioxidative biomarkers, restoring cellular redox balance. Results: Our findings suggest that Prgn exerts neuroprotective effects against 6-OHDA-induced neurotoxicity in SH-SY5Y cells by reducing oxidative stress and enhancing cell survival. These results support the exploration of Prgn as a potential therapeutic agent for mitigating PD progression. Conclusion: In conclusion, our study demonstrates that Prgn, a neurosteroid, exhibits promising neuroprotective effects in an in vitro model of PD by attenuating 6-OHDA-induced oxidative damage and preserving the viability and functional integrity of SH-SY5Y cells. [ABSTRACT FROM AUTHOR]

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The aim of this study was to investigate the molecular, biochemical, and histopathological effects of bromelain, which has antioxidant and anti-inflammatory properties, against cisplatin-induced ocular toxicity. The groups were designed as (1) Control, (2) Cisplatin (7 mg/kg, intraperitoneally), (3) Cisplatin + Bromelain (50 mg/kg, orally for 14 consecutive days), (4) Cisplatin + Bromelain (100 mg/kg, orally for 14 consecutive days). The activity of total antioxidant capacity (TAC) and total oxidant status (TOS) and levels of reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), interleukin-1β (IL-1β), IL-10, nuclear factor kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α) and 8-OHdG were measured in ocular tissue. The mRNA expression of NF-κB and Caspase-3 was also evaluated. Also, ocular sections were evaluated histopathologically. Bromelain demonstrated a dose-dependent protective effect in cisplatin-induced toxicity by regulating oxidative stress, inflammation, and tissue damage. Our results suggested that bromelain may be a potential adjuvant that can protect the eye from cisplatin-induced toxicity. [ABSTRACT FROM AUTHOR]

Current study was designed to investigate the protective effects of etanercept in glutamate excitotoxicity in rat neuronal culture through anti-inflammatory and anti-oxidant mechanisms. Rat cortical neurons were exposed to glutamate and to assess the effect of etanercept in glutamate toxicity, etanercept was applied at various doses (0.1, 0.5, 1, 10 µg/ml). Then we examined the changes in neuronal cell viability, oxidative stress and inflammation. Etanercept preserved cultured cells from glutamate excitotoxicity. Our cell viability analysis (3-(4,5-Dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide and lactate dehydrogenase) revealed that etanercept markedly increased the viability ratio of neurons injured by glutamate. In addition, the potential antioxidant property of etanercept was evaluated via the examination of oxidative stress parameters, such as MDA and TOS, and antioxidant parameters measured as TAS and SOD. Moreover, TNF-𝛼 levels were measured to evaluate anti-inflammatory effects of etanercept. Obtained data proved that etanercept increases the activity of the antioxidative parameters while decreased oxidative parameters and inflammation. The current study demonstrated that etanercept strongly prevents glutamate- induced neuronal cell death. This study is the first to demonstrate a potential protective effect of etanercept in neurons exposed to glutamate excitotoxicity and opens new doors on the therapeutic potential of etanercept. [ABSTRACT FROM AUTHOR]

To investigate the effect of taxifolin on cisplatin-induced oxidative and proinflammatory optic nerve damage in rats. A total of 18 albino Wistar male rats were assigned into 3 groups, as follows; Group 1: Control group, Group 2: Only cisplatin administered group for 14 days (Cisplatin group), and Group 3: Taxifolin + cisplatin administered group for 14 days (CIS + TAX group). Serum malondialdehyde (MDA), total Glutathione (tGSH), Nuclear Factor-Kappa B (NF-ƘB), Total Oxidative Status (TOS) and Total Antioxidant Status (TAS) levels were collected from the left eyes of rats. Rats' right eyes were enucleated for histopathological evaluations of optic nerves. NF-ƘB, MDA and TOS levels were statistically significantly higher (p < 0.001) in cisplatin group when compared to other 2 groups, the tGSH and TAS levels of which were statistically significantly lower (p < 0.001). Regarding these parameters, in cisplatin group NF-ƘB, MDA and TOS levels were statistically significantly increased with cisplatin administration and giving taxifolin concomitantly with cisplatin prevented this elevation. On the other hand, tGSH and TAS levels were statistically significantly decreased with cisplatin administration and routine simultaneous application of taxifolin with cisplatin prevented this decrease. In histopathological findings, haemorrhage was observed in the perineum of the injured optic nerves in the cisplatin treated group. And also edoema and degeneration in nerve fascicles in damaged optic nerves were seen in the cisplatin group. In the taxifolin treated group histopathological examinations were close to normal appearance, except mild edoema in nerve fascicles. Cisplatin causes oxidative stress on the rat optic nerves, and these changes lead to significant histopathological damage. Taxifolin, which we used to prevent oxidative damage to the optic nerves caused by cisplatin, has been emphasized as a powerful antioxidant agent in many previous scientific investigations. Concomitant administration of taxifolin may prevent these adverse effects of cisplatin, as well as histopathological damage. Further studies are needed to fully determine the effects of cisplatin and taxifolin on the eye. [ABSTRACT FROM AUTHOR]