The Potential Anti-Cancer Effects Of Psidium Guajava (Guava) Leaves On Coloretal Cancer Via The Inhibition Of Angiogenesis

Colorectal cancer, which is the cancer that develops in the colon or rectum, is one of the most common cancers that lead to death. The prevalence of colorectal cancer in Malaysia is expected to increase due to the aging population, socioeconomic advances, and increasingly Westernised diet and lifestyle. The growth of colorectal tumours beyond a certain size, as well as their metastatic spread, is dependent on the increase in angiogenesis of their surrounding vasculature. As Psidium guajava (guava) leaves are rich in phenolic compounds, flavonoids, carotenoids, and vitamins, the anti-angiogenic and anticancer activities of P. guajava leaf extracts were investigated to assess their potential in the treatment of the angiogenesis-dependent colorectal cancer. Three extracts were produced using distilled water, ethanol, and n-hexane as solvents, and were labelled as dH2O, EOH, and NH. The extracts were physically characterised through gas chromatography–mass spectrometry (GC-MS), ultraviolet-visible spectroscopy (UV-Vis), and Fourier transform infrared spectroscopy (FTIR). Through the DPPH radical scavenging, total phenolic content, and total flavonoid content assays, the EOH extract was found to have the highest antioxidant activity. The dH2O and EOH extracts exhibited more inhibitory activity against EA.hy926 (human vascular endothelial) cell viability and microvessel growth from rat aortic rings compared to the NH extract, indicating a better anti-angiogenic activity

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

The Anticancer Potential of <i>Psidium guajava</i> (Guava) Extracts

The fruits, leaves, and bark of the guava (Psidium guajava) tree have traditionally been used to treat a myriad of ailments, especially in the tropical and subtropical regions. The various parts of the plant have been shown to exhibit medicinal properties, such as antimicrobial, antioxidant, anti-inflammatory, and antidiabetic activities. Recent studies have shown that the bioactive phytochemicals of several parts of the P. guajava plant exhibit anticancer activity. This review aims to present a concise summary of the in vitro and in vivo studies investigating the anticancer activity of the plant against various human cancer cell lines and animal models, including the identified phytochemicals that contributes to their activity via the different mechanisms. In vitro growth and cell viability studies, such as the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, the sulforhodamine B (SRB) assay, and the trypan blue exclusion test, were conducted using P. guajava extracts and their biomolecules to assess their effects on human cancer cell lines. Numerous studies have showcased that the P. guajava plant and its bioactive molecules, especially those extracted from its leaves, selectively suppress the growth of human cancer cells without cytotoxicity against the normal cells. This review presents the potential of the extracts of P. guajava and the bioactive molecules derived from it, to be utilized as a feasible alternative or adjuvant treatment for human cancers. The availability of the plant also contributes towards its viability as a cancer treatment in developing countries

The effect of Aflatoxin B1 on tumor-related genes and phenotypic characters of MCF7 and MCF10A cells

The fungal toxin aflatoxin B1 (AB1) and its reactive intermediate, aflatoxin B1-8, 9 epoxide, could cause liver cancer by inducing DNA adducts. AB1 exposure can induce changes in the expression of several cancer-related genes. In this study, the effect of AB1 exposure on breast cancer MCF7 and normal breast MCF10A cell lines at the phenotypic and epigenetic levels was investigated to evaluate its potential in increasing the risk of breast cancer development. We hypothesized that, even at low concentrations, AB1 can cause changes in the expression of important genes involved in four pathways, i.e., p53, cancer, cell cycle, and apoptosis. The transcriptomic levels of BRCA1, BRCA2, p53, HER1, HER2, cMyc, BCL2, MCL1, CCND1, WNT3A, MAPK1, MAPK3, DAPK1, Casp8, and Casp9 were determined in MCF7 and MCF10A cells. Our results illustrate that treating both cells with AB1 induced cytotoxicity and apoptosis with reduction in cell viability in a concentration-dependent manner. Additionally, AB1 reduced reactive oxygen species levels. Phenotypically, AB1 caused cell-cycle arrest at G1, hypertrophy, and increased cell migration rates. There were changes in the expression levels of several tumor-related genes, which are known to contribute to activating cancer pathways. The effects of AB1 on the phenotype and epigenetics of both MCF7 and MCF10A cells associated with cancer development observed in this study suggest that AB1 is a potential risk factor for developing breast cancer