Omeprazole and Spirulina Platensis Ameliorate Steatohepatitis in Experimental Nonalcoholic Fatty Liver Disease.

Background: Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage, and it affects about 24% of the population worldwide. This study aimed to investigate the effect of omeprazole and Spirulina platensis on hepatic and serum biochemical alterations in NAFLD induced by high-fat diet (HFD). Methods: Male Wistar rats were divided into four groups; one served as a normal control. The other groups received HFD and subdivided into three subgroups; one was left untreated and the other two groups were treated orally with either omeprazole (10 mg/kg) or Spirulina (1000 mg/kg) for 30 consecutive days. Results: Omeprazole successfully decreased elevated serum pentraxin-3 (PTX-3) and cytokeratin-18 (CK-18) levels and hepatic sterol regulatory element binding protein-1c (SREBP-1c) expression, while Spirulina had better impact on decreasing liver function enzymes, lipid profile, and nuclear factor erythroid 2-related factor 2 (Nrf-2) levels compared to omeprazole. Both treatments had similar effects on normalizing glucose homeostasis, decreasing insulin resistance, and improving adipocytokine levels. Conclusion: Effects of omeprazole and Spirulina on markers of NAFLD appeared to be mediated by regulation of inflammatory, apoptotic, and oxidative mediators. Thus, omeprazole and Spirulina may find use as promising adjuvant therapy to ameliorate NAFLD. Research ethical committee of the faculty of pharmacy, Cairo University approved the research (BC 1479).

Impact of betanin against paracetamol and diclofenac induced hepato-renal damage in rats.

Context: Paracetamol (PAR) and diclofenac (DF) are the most popular consumed analgesics and anti-inflammatory medications.Objective: This study aimed to explore the protective effect of betanin (Bet) against PAR or DF induced hepato-renal damage in rats.Methods: Rats were randomly divided into five groups: Normal control (NC) group rats were given saline only. PAR group rats received PAR (400 mg/kg). PAR/Bet treated group rats administered PAR (400 mg/kg) plus Bet (25 mg/kg). DF group rats received DF (10 mg/kg). DF/Bet treated group rats administered DF (10 mg/kg) plus Bet (25 mg/kg). All drugs were given by gavage for 28 consecutive days.Results: PAR and DF administration in high dose and long-time induced liver and kidney injury, disrupted serum lipid profile, enhanced serum levels of inflammatory and oxidative stress markers, triggered DNA fragmentation and caused drastic changes in the histopathological pictures of the two organs. Bet supplementation succeeded to ameliorate most of the biochemical changes and protected DNA from damage as obtained from comet assay. Histological features in H&E taken to different groups also mirrors this findings.Conclusion: Bet exerted a potential anti-inflammatory and antioxidant effect against hepato-renal damage induced by PAR or DF overconsumption.

Protective effects of betanin against paracetamol and diclofenac induced neurotoxicity and endocrine disruption in rats.

Context: Overconsumption of paracetamol (PAR) and diclofenac (DF) have been reported to induce neurotoxicity and endocrine disruption. Objective: The current study was designed to explore the protective potential of betanin against PAR and DF inducing neurotoxicity and endocrine disruption in a rat model. Material and Methods: Forty rats were equally divided into five groups: group I served as control, group II received PAR (400 mg/kg), group III received PAR plus betanin (25 mg/kg), group IV received DF (10 mg/kg) and group V received DF plus betanin orally for 28 consecutive days. Thyroid axis hormones, sex hormone, neurotransmitters, paraoxonase-1, hemeoxygenase-1 and nuclear factor-2 were measured by ELISA. While, the oxidative stress markers were colorimetrically estimated. Moreover, DNA damage and histopathological picture of the brains were investigated. Results: A marked reduction in thyroid axis hormones, brain neurotransmitters and serum testosterone as well as enhanced oxidative stress and brain DNA damage accompanied by drastic changes in the brain histopathological picture were recorded in the challenged PAR and DF groups. Betanin supplementation ameliorated most of the biochemical and histopathological changes induced by PAR or DF. Conclusion: The study suggests betanin of potential protective effects against neurotoxicity and endocrine disruption induced by PAR and DF overconsumption.

Protective effect of ellagic acid and pumpkin seed oil against methotrexate-induced small intestine damage in rats.

Gastrointestinal toxicity is one of the most serious side effects in the methotrexate (MTX) treatment. This study was designed to investigate whether ellagic acid (EA) and/or pumpkin seed oil (PSO) had a protective effect on MTX-induced small intestine damage. Forty albino rats were randomized into five groups of 8 rats each. Group I served as a normal control group. In Group II, MTX was administered as a single dose (20 mg/kg) intraperitoneally. Groups III, IV and V were pre-treated respectively with either PSO (40 mg/kg), EA (10 mg/kg) or 0.2% DMSO (vehicle control) orally every day by gavage for 5 days and then they received MTX. All animals were sacrificed 5 days after the intraperitoneal injection of MTX for histopathological examination, estimation of serum prostaglandin E2 (PGE2) level, assay of tissue malondialdehyde (MDA), reduced glutathione (GSH) and nitric oxide (NO) levels and myloperoxidase (MPO), xanthine oxidase (XO) and adenosine deaminase (AD) activities. Administration of EA and/or PSO decreased the intestinal damage, PGE2, MDA and NO levels and MPO, XO and AD activities and increased GSH level. These results suggest that EA and PSO protect the small intestine of rats from MTX-induced damage through their antioxidant and anti-inflammatory effects and thus have potential as a promising drug in the prevention of undesired side effects of MTX.