Bromelain protects against cisplatin-induced ocular toxicity through mitigating oxidative stress and inflammation.
Irmak Ferah OkkayUfuk OkkayCemil BayramBetul CicekSelma SezenIsmail Cagri AydinAli Sefa MendilAhmet HacimuftuogluPublished in: Drug and chemical toxicology (2021)
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.
Keyphrases
- oxidative stress
- nuclear factor
- induced apoptosis
- dna damage
- reactive oxygen species
- toll like receptor
- diabetic rats
- anti inflammatory
- ischemia reperfusion injury
- rheumatoid arthritis
- cell death
- optic nerve
- signaling pathway
- early stage
- heat shock
- hydrogen peroxide
- lps induced
- breast cancer cells
- cell proliferation
- pi k akt
- immune response
- single molecule
- cell cycle arrest
- climate change