The aim of the current study was to test the hypothesis that forest bathing would be beneficial for elderly patients with chronic heart failure (CHF) as an adjunctive therapy. Two groups of participants with CHF were simultaneously sent to the forest or an urban control area for a four-day trip, respectively. Subjects exposed to the forest site showed a significant reduction of brain natriuretic peptide (BNP) in comparison to that of the city group and their own baseline levels. The values for the cardiovascular disease related pathological factors, including endothelin-1 (ET-1), and constituents of the renin-angiotensin system (RAS), including renin, angiotensinogen (AGT), angiotensin II (ANGII), and ANGII receptor type 1 or 2 (AT1 or AT2) in subjects exposed to the forest environment were lower than those in the urban control group. Obviously, a decreased level of inflammatory cytokines and improved antioxidant function was observed in the forest group rather than in the city group. The assessment of the profile of mood states (POMS) indicated that the negative emotional mood state was alleviated after forest bathing. As anticipated, a better air quality in the forest site was observed according to the detection of PM_2.5 (particulate matter <2.5 μm) and negative ions. These results provided direct evidence that forest bathing has a beneficial effect on CHF patients, and thus may pave the way for potential development of forest bathing as an effective adjunctive therapy on cardiovascular disorders.

The DNA damage response (DDR) is a signaling cascade that is triggered by DNA damage, involving the halting of cell cycle progression and repair. It is a key event leading to senescence, which is characterized by irreversible cell cycle arrest and the senescence-associated secretory phenotype (SASP) that includes the expression of inflammatory cytokines. Human cytomegalovirus (HCMV) is a ubiquitous pathogen that plays an important role in the senescence process. It has been established that DDR is necessary for HCMV to replicate effectively. This paper reviews the relationship between DDR, cellular senescence, and HCMV, providing new sights for virus-induced senescence (VIS).

Varicella-zoster virus (VZV), a member of the α-herpesvirus family, is known for causing two distinct diseases: chickenpox (varicella) during the primary infection and shingles (zoster) due to reactivation of the virus later in life. Although there are vaccines available to prevent VZV infection, it is still not universally effective, and antiviral treatments for VZV are limited and may come with significant side effects. Thus, development of novel therapeutics is urgently needed. We identified a naturally occurring Alantolactone (ALT) that inhibited replication of recombinant VZV in human diploid fibroblast (WI-38 cells) and Adult Retinal Pigment Epithelial cell line-19 (ARPE-19 cells) through Western blotting, qPCR and plaque assays. Subsequently, we explored the mechanism underlying the anti-VZV activity of ALT using time-of-addition experiments and transcriptomic analyses. A screening model was established for anti-VZV compounds, and we screened ALT was with good anti-VZV efficacy. Our findings revealed that ALT alleviated cytopathic changes, reduced viral titres, and inhibited the expression of viral genes and proteins in WI-38 cells and ARPE-19 cells. Furthermore, our data showed that ALT inhibited VZV infection in intracellular viral replication. Finally, multiple inflammatory pathways were involved in the antiviral role of ALT, and IL-6 was one of the most critical hub genes. Together, our findings identify ALT as an anti-VZV agent that may prove useful in the treatment of VZV replication.

Human cytomegalovirus (HCMV) infection is responsible for congenital infections and poses a significant health risk to immunocompromised individuals. To da

This study presents the first investigation of acetyl-11-keto-β-boswellic acid (AKBA)’s anti-human cytomegalovirus (HCMV) activity in vitro and elucidates its underlying mechanisms. In HCMV Towne strain-infected WI-38 cells, AKBA (1-12 μM) exhibited negligible cytotoxicity while significantly suppressing virus-induced cytopathic effects (CPE) at 6–10 μM, with dose-dependent reduction of viral proteins (IE1/2 and p52) expression, viral DNA copy number (UL123, UL44, and UL32), and infectious viral progeny titer (TCID50). Time-of-addition experiments demonstrated the primary antiviral activity of AKBA during post-entry phase, along with direct virion inactivation. Transcriptome analysis revealed that AKBA significantly downregulated the expression of the host factor NR4A1 induced by HCMV, a finding further validated by Western blotting. Further gene knockdown experiments confirmed that silencing NR4A1 significantly reduced the expression of viral proteins IE1/2, thereby validating NR4A1 as a key host factor for HCMV infection. These findings indicate that AKBA has a potent and dose-dependent inhibitory effect on HCMV replication in WI-38 cells, and proves that this effect is mediated through two different mechanisms: one is the downregulation of the expression of the key host factor NR4A1, and the other is the direct inactivation of HCMV viral particles.