Green tea extract reduces viral proliferation and ROS production during Feline Herpesvirus type-1 (FHV-1) infection

被引:2
作者
Longobardi, Consiglia [1 ]
Damiano, Sara [1 ]
Ferrara, Gianmarco [1 ]
Esposito, Riccardo [1 ]
Montagnaro, Serena [1 ]
Florio, Salvatore [1 ]
Ciarcia, Roberto [1 ]
机构
[1] Univ Naples Federico II, Dept Vet Med & Anim Prod, Via F Delpino 1, I-80137 Naples, Italy
关键词
Feline Herpesvirus type-1; Green tea extract; ROS; Antiviral; OCULAR MANIFESTATIONS; SIMPLEX-VIRUS; CATECHINS; CATS; ANTIBACTERIAL; CALICIVIRUS; PREVALENCE; DIAGNOSIS;
D O I
10.1186/s12917-024-04227-0
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
Background Feline Herpesvirus type-1 (FHV-1) is a worldwide spread pathogen responsible for viral rhinotracheitis and conjunctivitis in cats that, in the most severe cases, can lead to death. Despite the availability of a variety of antiviral medications to treat this illness, mainly characterized by virostatic drugs that alter DNA replication, their use is often debated. Phytotherapeutic treatments are a little-explored field for FHV-1 infections and reactivations. In this scenario, natural compounds could provide several advantages, such as reduced side effects, less resistance and low toxicity. The purpose of this study was to explore the potential inhibitory effects of the green tea extract (GTE), consisting of 50% of polyphenols, on FHV-1 infection and reactive oxygen species (ROS) production. Results Crandell-Reese feline kidney (CRFK) cells were treated with different doses of GTE (10-400 mu g/mL) during the viral adsorption and throughout the following 24 h. The MTT and TCID50 assays were performed to determine the cytotoxicity and the EC50 of the extract, determining the amounts of GTE used for the subsequent investigations. The western blot assay showed a drastic reduction in the expression of viral glycoproteins (i.e., gB and gI) after GTE treatment. GTE induced not only a suppression in viral proliferation but also in the phosphorylation of Akt protein, generally involved in viral entry. Moreover, the increase in cell proliferation observed in infected cells upon GTE addition was supported by enhanced expression of Bcl-2 and Bcl-xL anti-apoptotic proteins. Finally, GTE antioxidant activity was evaluated by dichloro-dihydro-fluorescein diacetate (DCFH-DA) and total antioxidant capacity (TAC) assays. The ROS burst observed during FHV-1 infection was mitigated after GTE treatment, leading to a reduction in the oxidative imbalance. Conclusions Although further clinical trials are necessary, this study demonstrated that the GTE could potentially serve as natural inhibitor of FHV-1 proliferation, by reducing viral entry. Moreover, it is plausible that the extract could inhibit apoptosis by modulating the intrinsic pathway, thus affecting ROS production.
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