Search

Aging and aging-related diseases present a global public health problem. Therefore, the development of efficient anti-aging drugs has become an important area of research. Traditional Chinese medicine is an important complementary and alternative branch of aging-related diseases therapy. Recently, a growing number of studies have revealed that traditional Chinese medicine has a certain delaying effect on the progression of aging and aging-related diseases. Here, we review the progress in research into using traditional Chinese medicine for aging and aging-related diseases (including neurodegenerative diseases, cardiovascular diseases, diabetes, and cancer). Furthermore, we summarize the potential mechanisms of action of traditional Chinese medicine and provide references for further studies on aging and aging-related diseases. [ABSTRACT FROM AUTHOR]

Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development. [ABSTRACT FROM AUTHOR]

Background: Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread rapidly to become a global pandemic. Opportunistic infections (OIs) are common in patients with acquired immunodeficiency syndrome (AIDS). Mycobacterium avium complex (MAC) and oral candidiasis (OC) are frequently responsible for such infections. Here, we describe a patient with a recent history of COVID-19 who was also diagnosed with human immunodeficiency virus (HIV), MAC, and OC. Case Presentation: The patient was a 23-year-old woman with a past medical history of HIV infection who was diagnosed with SARS-CoV-2 infection 6 days prior to her referral to hospital. Her chief complaints were chest distress and continuous fever with a background of a 5-month history of anemia and tuberculosis (TB). Chest X-ray showed bilateral parenchymal infiltrates suspicious for COVID-19. She was treated with oxygen, empiric antibacterial and antiretroviral therapy. Further workup showed MAC and OC infection. She was started on ethambutol, rifampin and antifungal treatment for influenzas and her symptoms resolved in 8 weeks. Follow-up chest computed tomography scanning showed that the lung lesions disappeared within a short period of time. Conclusion: A thorough history and clinical examination are vital to arriving at the correct diagnosis or diagnoses. With the COVID-19 pandemic, clinicians caring for immunosuppressed patients need to remain vigilant of the simultaneous presence of OIs. This report highlights the importance of the treatment and prevention of OIs in HIV-infected persons, which may reduce adverse consequences after infection with SARS-CoV-2. [ABSTRACT FROM AUTHOR]

This study aimed to explore the survival of AIDS patients treated with traditional Chinese medicine (TCM) in addition to combined antiretroviral therapy (cART) and of AIDS patients treated with cART. Data of patients taking cART between 30 October 2003 and 30 October 2004 in the National TCM HIV Treatment Trial Program area were retrospectively analyzed, with follow-up from 30 October 2004 to 30 October 2012. The log-rank test was used to compare survival between the two groups. A Cox proportional hazards model was used to determine hazard ratios to identify prognostic factors. The study included 521 patients in the TCM + cART group followed up for 3548 person-years and 375 patients in the cART group followed up for 2523 person-years. Mortality rates were 3.2/100 person-years and 4.2/100 person-years in the TCM + cART and cART groups, respectively. The difference in survival was significant. After adjusting for explanatory variables, the mortality rate of AIDS patients in the cART group was 1.7 times higher than in the TCM + cART group. Male sex, older age, little education, and lower CD4 cell count were risk factors for mortality. TCM intervention in addition to cART could increase survival of AIDS patients. [ABSTRACT FROM AUTHOR]

A retrospective cohort study was conducted to explore the effectiveness of Traditional Chinese Medicine (TCM) in treating people living with HIV (PLHIV) by comparing the survival of PLHIV treated with TCM and without TCM. To identify prognostic factors that affect the survival of PLHIV, patients who enrolled in the national TCM HIV treatment trial program (NTCMTP) in October 2004 and PLHIV in the same region who did not enroll in the NTCMTP were compared. Participants were followed up to October 2012. Survival time was estimated through the Kaplan-Meier method, and hazard ratios to identify prognostic factors were computed through Cox proportional hazard models. A total of 3,229 PLHIV (1,442 in the TCM therapy group and 1,787 in the non-TCM therapy group) were followed up for 21,876 person-years. In this time period, 751 (23.3%) died and 209 (6.5%) were lost to follow-up, for an overall mortality rate of 3.43/100 person-years. In the TCM therapy group, 287 (19.0%) died and 139 (9.7%) were lost to follow-up, and in the non-TCM therapy group, 464 (26.0%) PLHIV died and 70 (3.9%) were lost to follow-up. The mortality rate in the TCM therapy group was 2.97/100 person-years, which was lower than the rate of 3.79/100 person-years in the non-TCM therapy group. The 8-year cumulative survival in the TCM therapy group was 78.5%, lower than the 74.0% survival in the non-TCM therapy group. After adjusting for other factors, risk factors of death included male gender, older age, less education, taking combined antiretroviral therapy (cART) at enrollment, not taking cART at follow-up, and lower CD4 + T cell counts. Our retrospective cohort study indicates that TCM increased the survival and lengthened the lifetime of PLHIV in Henan Province of China. However, the limitations of a retrospective cohort could have biased the study, so prospective studies should be carried out to confirm our primary results. [ABSTRACT FROM AUTHOR]

Progastrin-releasing peptide (ProGRP), which is known to be highly specific and sensitive to small cell lung cancer (SCLC), has been proven to be a valuable substitute for neuron-specific enolase in SCLC diagnostics and monitoring, especially in its early stages. The detection of ProGRP levels also facilitates a selection of therapeutic treatments. For the fabrication of our proposed biosensor, titanium (IV) oxide microparticles were first used, followed by dispersing gold nanoparticles into chitosan and immobilizing them onto a carbon paste electrode (CPE) surface. The developed immunosensor exhibits a much higher biosensing performance in comparison with current methods, when it comes to the detection of ProGRP. Therefore, the proposed CPE/TiO2/(CS+AuNPs)/anti-ProGRP/BSA/ProGRP is excellent for the development of a compact diagnostics apparatus. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a serious public health concern. Excessive inflammatory responses of vascular cells are considered a pivotal pathogenesis mechanism underlying atherosclerosis development. It is known that Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signalling plays an important role in atherosclerosis progression. Protein inhibitor of activated STAT3 (PIAS3) is the key negative regulator of JAK/STAT3 signalling. However, its effect on atherogenesis is unknown. Here, we observed that PIAS3 levels are reduced in atherosclerotic lesions and that PIAS3 expression decreases in conjunction with increases in interleukin-6 expression and atherosclerosis severity. Oxidized low-density lipoprotein (ox-LDL), an atherogenic stimulus, reduced PIAS3 expression, an effect that may be attributed to nitric oxide synthesis upregulation. In turn, PIAS3 overexpression effectively suppressed ox-LDL-induced inflammation, lipid accumulation and vascular smooth muscle cell proliferation. These results indicate that PIAS3 is a critical repressor of atherosclerosis progression. The findings of this study have contributed to our understanding on the pathogenesis of atherosclerosis and have provided us with a potential target through which we can inhibit atherosclerosis-related cellular responses. [ABSTRACT FROM AUTHOR]

Porcine reproductive and respiratory syndrome virus (PRRSV) causes inflammatory injuries in infected pigs. PRRSV induces secretion of high mobility group box 1 (HMGB1) that enhances inflammatory response. However, the mechanism of PRRSV-induced HMGB1 secretion is unknown. Here, we discovered PRRSV induced HMGB1 secretion via activating protein kinase C-delta (PKCδ). HMGB1 secretion was positively correlated with PKCδ activation in PRRSV-infected cells in a dose and time-dependent manner. Suppression of PKCδ with inhibitor and siRNA significantly blocked PRRSV-induced HMGB1 translocation and secretion, which indicates PKCδ activation is essential for the PRRSV-mediated HMGB1 secretion. In addition, PKCδ knockdown in PRRSV-infected cells led to downregulation of inflammatory cytokines, including IL-1beta and IL-6. Moreover, PRRSV E and pORF5a proteins were found to activate PKCδ and consequent HMGB1 secretion. These results demonstrate PRRSV activates PKCδ to induce HMGB1 secretion via E and pORF5a. This finding provides insights on the inflammatory response and pathogenesis of PRRSV infection. [ABSTRACT FROM AUTHOR]