RNA-Seq analysis on effects of royal jelly on tumour growth in 4T1-bearing mice

Zhang, Shuang; Nie, Hongyi; Shao, Qiqi; Hassanyar, Aqai Kalan; Su, Songkun

doi:10.1016/j.jff.2017.07.010

Cited by 4 publications

(1 citation statement)

References 42 publications

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“…RJ is a mixture of free amino acids, proteins, sugars, lipids, vitamins, and minerals (Ahmed et al, 2014). RJ exhibits anti-oxidant (Abdel-Hafez et al, 2017), anti-inflammatory (Karaca et al, 2012), immunomodulatory (El-Nekeety et al, 2007), anti-tumor (Zhang et al, 2017), anti-hypercholesterolemic (Ibrahim, 2014), anti-microbial (Chan et al, 2009) and anti-allergic (Oka et al, 2001) activities. Moreover, RJ has shown neuroprotective effects in stress-induced animal models (Teixeira et al, 2017), aging (Pyrzanowska et al, 2014), and drug-induced neurotoxicity (Mohamed et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of royal jelly against diclofenac-induced hepato-renal damage and gastrointestinal ulcerations in rats

Mostafa

El-Marasy

Jaleel

et al. 2020

Heliyon

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Evaluation of traditionally used royal jelly (RJ) for the management of hepato-renal damage and gastrointestinal ulcerations caused by diclofenac. Methods: Forty adult male Wistar rats were allocated into four groups. Rats of the 1 st group received only saline and served as normal group. The remaining 3 groups received diclofenac (50 mg/kg/day, I.P.) for 7 days. Group 2 served as diclofenac-control group. Groups 3 and 4 received RJ (150 and 300 mg/kg/day, P.O.) respectively for 30 days. Twenty-four hours after the last treatment, blood samples were collected, rats were sacrificed, and livers, kidneys, stomachs & intestines were harvested. Stomachs and intestines were tested for ulcer counts. Serum levels of AST, ALT, creatinine and urea were investigated. Hepatic, renal, gastric and intestinal tissue contents of myeloperoxidase (MPO) and prostaglandin-E2 (PGE2) were measured. Histopathological examinations were also performed followed by immunohistochemical determination of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression. Results: Diclofenac administration caused significant deterioration of all the above mentioned parameters. RJ improved hepatic and renal functions. Gastric and intestinal ulcer counts were significantly ameliorated. Hepatic, renal, gastric and intestinal tissue PGE-2 contents and COX-2 expression were significantly elevated. RJ also significantly reduced MPO content and iNOS expression as compared to diclofenac-control group. Improvements of the histopathological pictures of hepatic, renal, gastric and intestinal tissues were also apparent. Conclusion:The study demonstrates promising protective effects of RJ against diclofenac-induced hepato-renal damage and gastrointestinal ulceration in rats.

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