Acyclovir is a potent oral antiviral drug. Acyclovir has anti-herpetic activity with IC50 values of 0.85 μM and 0.86 μM for HSV-1 and HSV-2, respectively. Acyclovir induces cell cycle disruption and apoptosis[1] [2].
In the plaque reduction assay (PRA) of Vero cells, Acyclovir (20μM; 3d) treatment showed 100% plaque inhibition[1]. Acyclovir (10-100μM; 24-72h) blocks DNA synthesis, thereby arresting the cell cycle at G2/M and S phases and increasing the G1 hypodiploid peak in a dose-dependent manner. Acyclovir (10-100μM; 24-72h) induces apoptosis through activation of caspase-3 and the presence of nuclear DNA fragmentation[2].
Treatment of infected mice with Acyclovir (20mg/kg; po; three times daily; 10d) inhibited the development of skin lesions and led to a dissociation between the DTH response and antibody production [3]. In the Acyclovir-induced nephrotoxicity model, after mice were given Acyclovir (150, 600 mg/kg; ip; 9d), serum creatinine and urea nitrogen levels increased, histopathological changes occurred in the kidneys of mice, and the expression levels of vascular endothelial growth factor (VEGF) and its receptor VEGFR2 were reduced[4].
References:
[1]. Musarra-Pizzo M, Pennisi R, Ben-Amor I, et al. In vitro anti-HSV-1 activity of polyphenol-rich extracts and pure polyphenol compounds derived from pistachios kernels (Pistacia vera L.)[J]. Plants, 2020, 9(2): 267.
[2].Suzuki M, Okuda T, Shiraki K. Synergistic antiviral activity of Acyclovir and vidarabine against herpes simplex virus types 1 and 2 and varicella-zoster virus[J]. Antiviral research, 2006, 72(2): 157-161.
[3]. Benedetti S, Catalani S, Palma F, et al. Acyclovir induces cell cycle perturbation and apoptosis in Jurkat leukemia cells, and enhances chemotherapeutic drug cytotoxicity[J]. Life sciences, 2018, 215: 80-85.
[4].Lu H, Han Y J, Xu J D, et al. Proteomic characterization of acyclovir-induced nephrotoxicity in a mouse model[J]. PLoS One, 2014, 9(7): e103185.
Acyclovir是一种强效的口服抗病毒药物。Acyclovir具有抗疱疹活性，对 HSV-1 和 HSV-2 的 IC50 值分别为 0.85μM 和 0.86μM。Acyclovir诱导细胞周期紊乱和细胞凋亡[1] [2]。
Vero 细胞的噬斑减少试验（PRA）中，Acyclovir（20 μM；3 天）治疗显示 100% 斑块抑制作用[1]。Acyclovir（10-100μM；24-72h）阻断DNA合成，从而将细胞周期停滞在G2/M和S期，并以剂量依赖性方式增加 G1 亚二倍体峰。Acyclovir（10-100μM；24-72h）通过激活caspase-3和存在核 DNA 碎片来诱导细胞凋亡[2]。
Acyclovir（20mg/kg；po；three times daily；10d）治疗感染小鼠可抑制皮肤病变的发展，导致DTH反应与抗体产生之间的解离[3]。在Acyclovir诱导的肾毒性模型中，小鼠给予Acyclovir（150，600mg/kg；ip；9d）后，血清肌酐和尿素氮水平升高，小鼠肾脏出现组织病理学改变，血管内皮生长因子(VEGF)及其受体VEGFR2的表达水平降低[4]。