Browse Articles

Acquired drug resistance is an increasing challenge in treating cancer with chemotherapy. One mechanism
behind this resistance is the increased inflammation that supports the progression and development of
cancer that arises because of the drug’s presence. Integrative oncology is the field that focuses on including natural products alongside traditional therapy to create a treatment that focuses on holistic patient well-being.
In this study, the authors demonstrate that the use of an herbal formulation, consisting of turmeric and green tea, alongside a traditional chemotherapeutic drug, 5-fluorouracil (FU) significantly decreases the level of cytokines produced in breast cancer cells when compared to the levels produced when exposed solely to the chemo drug. The authors conclude that this combination of treatment, based on the principle of integrative oncology, shows potential for reducing the resistance against treatment conferred through increased inflammation. Consequently, this suggests a prospective way forward in improving the efficacy of cancer treatment.

The purpose of our study was to determine if direct administration of CXCL1/KC to cardiomyocytes causes negative changes to cell density or proliferation. This molecule has been shown to reduce inflammation in certain instances. Homocysteine models the direct effect of an inflammatory agent on cardiomyocytes. Our question was whether these molecules directly impact cell density through an interaction with the cell proliferation process. We hypothesized that cells treated with CXCL1/KC would maintain the same cell density as untreated cells. In contrast, cells treated with Homocysteine or both Homocysteine and CXCL1/KC, were expected to have a higher cell density that than that of untreated cells.

The authors looked at whether traditional Chinese medicine remedies that target the lungs and liver would reduce inflammation in a planaria model. They found that the two active compounds they tested were able to decrease induced inflammation by 97-98%.

Oxidative damage and neuro-inflammation were the key pathways implicated in the pathogenesis of Alzheimer’s disease. In this study, 30 natural extracts from plant roots and leaves with extensive anti-inflammatory and anti-oxidative properties were consumed by Drosophila melanogaster. Several assays were performed to evaluate the efficacy of these combinational extracts on delaying the progression of Alzheimer’s disease. The experimental group showed increased motor activity, improved associative memory, and decreased lifespan decline relative to the control group.

The authors seek to accelerate wound healing by reducing inflammation with a cocktail containing growth factors and bioactive modulators.

Cell-free biologicals are a novel method of treating clinical conditions which involve chronic inflammation such as tendonitis and osteoarthritis. This study compared platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) in platelet-rich plasma (PRP), activated PRP (aPRP), and platelet lysate (PL). It was hypothesized that PL would contain higher concentrations of growth factors than PRP and that different storage temperatures for PL would diminish cytokine expression. Results demonstrated PL had the highest concentrations of both cytokines, with concentrations slightly diminishing at-80C. aPRP and PRP demonstrated lower concentrations of PDGF and VEGF than PL.

Wound-healing involves a sequence of events, such as inflammation, proliferation, and migration of different cell types like fibroblasts. Zinc Finger CCCH-type with G-Patch Domain Containing Protein (ZGPAT), encodes a protein that has its main role as a transcription repressor by binding to a specific DNA sequence. The aim of the study was to find out whether inhibiting ZGPAT will expedite the wound healing process by accelerating cell migration. This treatment strategy can provide a key to the development of wound healing strategies in medicine and cellular biology.

Tertiary lymphoid structures (TLS) are lymph node-like structures that form at sites of inflammation, and their presence in cancer patients is predictive of a better clinical outcome. One significant obstacle to TLS formation is reduced immune cell infiltration into the tumor microenvironment (TME). Recent studies have shown that vasculature normalizing (VN) agents may override this defect to improve tissue perfusion and increased immune cell entry into the TME. However, their effects on immune cell and tumor cell phenotype remain understudied. Here the authors investigate whether treating tumor cells with VN would reduce their immunosuppressive phenotype and promote production of chemokine that recruit immune cells and foster TLS formation.

Omega-3 fatty acid derived lipid mediators have been implicated in resolving inflammation, and wound healing. Authors measured the impact of supplementation with lipid mediator Resolvin D1 and its precursor 17-HDHA on planaria regeneration. Planaria not only synthesize RvD1 from 17-DHA, but both RvD1 and 17-DHA enhanced regeneration.

Anticholinergics are used in treating asthma, a chronic inflammation of the airways. These drugs block human M1 and M2 muscarinic acetylcholine receptors, inhibiting bronchoconstriction. However, studies have reported complications of anticholinergic usage, such as exacerbated eosinophil production and worsened urinary retention. Modification of known anticholinergics using bioisosteric replacements to increase efficacy could potentially minimize these complications. The present study focuses on identifying viable analogs of anticholinergics to improve binding energy to the receptors compared to current treatment options. Glycopyrrolate (G), ipratropium (IB), and tiotropium bromide (TB) were chosen as parent drugs of interest, due to the presence of common functional groups within the molecules, specifically esters and alcohols. Docking score analysis via AutoDock Vina was used to evaluate the binding energy between drug analogs and the muscarinic acetylcholine receptors. The final results suggest that G-A3, IB-A3, and TB-A1 are the most viable analogs, as binding energy was improved when compared to the parent drug. G-A4, IB-A4, IB-A5, TB-A3, and TB-A4 are also potential candidates, although there were slight regressions in binding energy to both muscarinic receptors for these analogs. By researching the effects of bioisosteric replacements of current anticholinergics, it is evident that there is a potential to provide asthmatics with more effective treatment options.