Anti-BAX polyclonal antibody

White spot syndrome virus (WSSV) causes high mortality in crustacean, but there are no effective therapies up to now. Medicinal plants and their bioactive ingredients are important sources of therapeutic agents. In the study, the anti-WSSV activities of 10 plant extracts were investigated in crayfish Procambarus clarkii. The results showed that the ethanol extracts of Eucommia ulmoides Oliver had the highest inhibition on WSSV replication among these tested extracts, with 84.12%. Geniposidic acid (GPA) is a major active ingredient of E. ulmoides. The contents of GPA in ethanol extracts of E. ulmoides were 32.148 mg/g. GPA could also suppress WSSV infection in vitro and in vivo. The inhibition rate was over 97% after treatment with 50 mg/kg GPA for 24 h. In addition, the mortality of WSSV-infected crayfish treated with GPA was 56.67%, while it was 100% for the controls. GPA possessed anti-inflammatory and anti-oxidative activities in crayfish. Mechanistically, GPA inhibited WSSV replication at least by reducing STAT expression to block the transcription of WSSV IE gene ie1. GPA also inhibited the expression of apoptosis related factor Bax inhibitor-1 which is beneficial for WSSV replication. In conclusion, GPA can be used as a potential agent to treat and prevent WSSV infection.

Aim: To investigate the possible modulatory effect of febuxostat in testosterone-induced benign prostatic hyperplasia (BPH) in rats with emphasis on xanthine oxidase (XO)/Janus Kinases (JAK)/signal transducer and activator of transcription (STAT) axis. Main methods: Male Wistar rats were treated with testosterone with/out febuxostat. Effect of febuxostat on BPH was assessed at the structural level by histopathology and determination of prostate weight/index. Cyclin Dl protein expression was assessed immunohistochemically and the ratio of Bax/Bcl-2 mRNA expression was determined by real time polymerase chain reaction analysis (RT-PCR). Besides, uric acid serum level was determined colorimetrically. Prostatic XO activity, as well as oxidative stress and inflammatory markers were evaluated. Additionally, western blot analysis was performed for determination of JAK-1 and phosphorylated form of STAT-3 expression in tissues. Key findings: Results revealed that febuxostat inhibited the increase in prostatic weight and index compared to testosterone-treated group. Additionally, febuxostat ameliorated testosterone-induced histopathological changes, prevented the rise in cyclin D1 expression and enhanced Bax/Bcl-2 ratio. Febuxostat suppressed testosterone induced- increase in XO activity in prostates and serum level of uric acid. Moreover, it regulated oxidative stress markers including; malondialdehyde (MDA), superoxide dismutase (SOD) activity and glutathione (GSH) content. Also, it inhibited the increase in prostate contents of interleukin-6 (IL-6), interleukin-113 (IL-1 beta), tumor necrosis factor (TNF-alpha) and nuclear factor (NF-kappa B). Interestingly, febuxostat markedly reduced JAK-1 and subsequent phosphorylation of STAT-3 protein expression. Significance: Febuxostat ameliorates testosterone-induced BPH via suppressing XO/JAK/STAT axis. This may help to re-purpose the use of XO inhibitors.