Phytochemical characterization, antioxidant and antibacterial activities of crude extracts of Anisomeles malabarica and Coldenia procumbens.

The aim of this study was to determine the phytochemical profile, antibacterial and antioxidant activities of crude aqueous leaf extracts of Anisomeles malabarica and Coldenia procumbens. The predominant components present in these crude extracts of test plants identified using gas chromatography-mass spectrometry (GC-MS) analysis in both plant extracts were phytochemicals including flavonoids, tannins, terpenoids, and phenols. The antibacterial activity of crude extracts of these plants against bacterial pathogens including Escherichia coli, Bacillus subtilis, Shigella sp., Salmonella paratyphi A and B, Proteus mirabilis, Proteus vulgaris, Pseudomonas sp. Klebsiella pneumoniae, and Staphylococcus aureus were examined. Data demonstrated that the extracts of A. malabarica and C. procumbens exhibited significant antibacterial activity against B.subtilis and P.vulgaris at the concentration of 50 mg/ml. A. malabarica aqueous extract displayed significant antioxidant activity on 2,2-diphenyl-1-picrylhydrazl (DPPH), fluorescence recovery after photobleaching (FRAP) and hydrogen peroxide (H2O2) free radicals at the concentration of 90 mg/ml. The antioxidant activity was significantly higher with A. malabarica than extract of C. procumbens. Evidence indicates that both plant extracts may possess significant pharmaceutical potential as antibacterial and antioxidant agents.

Antibacterial Mechanisms of Zinc Oxide Nanoparticle against Bacterial Food Pathogens Resistant to Beta-Lactam Antibiotics.

The increase in ß-lactam-resistant Gram-negative bacteria is a severe recurrent problem in the food industry for both producers and consumers. The development of nanotechnology and nanomaterial applications has transformed many features in food science. The antibacterial activity of zinc oxide nanoparticles (ZnO NPs) and their mechanism of action on ß-lactam-resistant Gram-negative food pathogens, such as Escherichia coli, Pseudomonas aeruginosa, Salmonella typhi, Serratia marcescens, Klebsiella pneumoniae, and Proteus mirabilis, are investigated in the present paper. The study results demonstrate that ZnO NPs possesses broad-spectrum action against these ß-lactamase-producing strains. The minimal inhibitory and minimal bactericidal concentrations vary from 0.04 to 0.08 and 0.12 to 0.24 mg/mL, respectively. The ZnO NPs elevate the level of reactive oxygen species (ROS) and malondialdehyde in the bacterial cells as membrane lipid peroxidation. It has been confirmed from the transmission electron microscopy image of the treated bacterial cells that ZnO NPs diminish the permeable membrane, denature the intracellular proteins, cause DNA damage, and cause membrane leakage. Based on these findings, the action of ZnO NPs has been attributed to the fact that broad-spectrum antibacterial action against ß-lactam-resistant Gram-negative food pathogens is mediated by Zn2+ ion-induced oxidative stress, actions via lipid peroxidation and membrane damage, subsequently resulting in depletion, leading to ß-lactamase enzyme inhibition, intracellular protein inactivation, DNA damage, and eventually cell death. Based on the findings of the present study, ZnO NPs can be recommended as potent broad-spectrum antibacterial agents against ß-lactam-resistant Gram-negative pathogenic strains.

Antimicrobial activity of nanoemulsion on drug-resistant bacterial pathogens.

The appearance of drug-resistant (DR) bacteria in the community is a crucial development, and is associated with increased morbidity, mortality, healthcare costs, and antibiotic use. Natural oil nanoemulsions (NEs) have potential for antimicrobial applications. In the present study, we determined the antimicrobial activity of an NE against DR bacterial pathogens in vitro. The NE comprised Cleome viscosa essential oil, Tween 80 nonionic surfactant, and water. We found that an NE with a droplet size of 7 nm and an oil:surfactant (v/v) ratio of 1:3 was effective against methicillin-resistant Staphylococcus aureus (MRSA), DR Streptococcus pyogenes, and DR extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Fourier-transform infrared (FTIR) spectroscopy revealed that NE treatment modified the functional groups of lipids, proteins, and nucleic acids in DR bacterial cells. Scanning electron microscopy (SEM) showed damage to the cell membranes and walls of NE-treated DR bacteria. These alterations were caused by bioactive compounds with wide-spectrum enzyme-inhibiting activity in the NE, such as ß-sitosterol, demecolcine, campesterol, and heneicosyl formate. The results suggest that the nanoemulsion is effective against DR bacteria, and acts by inhibiting the drug efflux mechanism of DR strains.

Exploring marine Lactobacillus and its protein for probiotic-based oral cancer therapy.

Cancer is a life-threatening malignancy and one of the leading global causes of human mortality. New approaches are required for cancer therapy due to the unique properties of cancer cells and the side effects of chemotherapy. Probiotics have gained significant attention in the prevention and treatment of various diseases, including cancer. Therefore, the current study aimed to investigate the anti-cancer effects of probiotics, such as marine Lactobacillus species and their proteins. Five marine Lactobacillus species were isolated and identified from the Tamil Nadu Mangrove Pichavaram (TLMP) forest and named TLMP1, TLMP2, TLMP3, TLMP4, and TLMP5. The Lactobacillus isolates, and their proteins were administered to male golden Syrian hamsters. Tumor formation was effectively controlled in hamsters treated with crude Lactobacillus, extending their lifespan. Additionally, Lactobacillus proteins demonstrated an inhibitory effect on tumor formation in the treated group compared to the control. Molecular docking analysis revealed that Lactobacillus proteins interacted significantly with the cAMP-dependent protein kinase catalytic subunit alpha. Amino acid residues LYS791, MET793, ARG841, ARG842, and LEU844 were involved in active site binding and played a crucial role in inhibiting cAMP-dependent protein kinase.

A review on tyrosine kinase inhibitors for targeted breast cancer therapy.

Breast cancer is a heterogeneous disease with complex molecular pathogenesis. Overexpression of several tyrosine kinase receptors is associated with poor prognosis, therefore, they can be key targets in breast cancer therapy. Tyrosine kinase inhibitors (TKIs) have emerged as leading agents in targeted cancer therapy due to their effectiveness in disrupting key molecular pathways involved in tumor growth. TKIs target various tyrosine kinases, including the human epidermal growth factor receptor 2 (HER2), epidermal growth factor receptor (EGFR), Vascular endothelial growth factor receptor (VEGFR), anaplastic lymphoma kinase (ALK), vascular endothelial growth factor receptor (VEGFR)-associated multi-targets, rearranged during transfection (RET), fibroblast growth factor receptor (FGFR), receptor tyrosine kinase-like orphan signal 1 (ROS1), Mitogen-activated protein kinase (MAPK), and tropomyosin receptor kinase (TRK). These drugs target the tyrosine kinase domain of receptor tyrosine kinases and play a vital role in proliferation and migration of breast cancer cells. Several TKIs, including lapatinib, neratinib, and tucatinib, have been developed and are currently used in clinical settings, often in combination with chemotherapy, endocrine therapy, or other targeted agents. TKIs have demonstrated remarkable benefits in enhancing progression-free and overall survival in patients with breast cancer and have become a standard of care for this population. This review provides an overview of TKIs currently being examined in preclinical studies and clinical trials, especially in combination with drugs approved for breast cancer treatment. TKIs have emerged as a promising therapeutic option for patients with breast cancer and hold potential for treating other breast cancer subtypes. The development of new TKIs and their integration into personalized treatment strategies will continue to shape the future of breast cancer therapy.

Identification of FOXM1 as a novel protein biomarker and therapeutic target for colorectal cancer progression: Evidence from immune infiltration and bioinformatic analyses.

Colorectal cancer (CRC) remains a major global health challenge, with its underlying molecular mechanisms, particularly the role of FOXM1, not yet fully understood. This study employed an integrated approach combining bioinformatics along with experimental validation to explore the role of FOXM1 in CRC. Using advanced computational tools and experimental techniques, we aimed to clarify the biological significance of FOXM1 and its potential impact on CRC progression and treatment. Bioinformatic analyses, including pan-cancer views, mRNA expression analysis, immune infiltrations, pathway enrichment, and functional annotations, highlighted the oncogenic potential of FOXM1 in CRC. Protein and gene expression analyses (western blot and qPCR) were conducted in HCT-116 and HT-29 cells. Platforms like GEPIA and UALCAN confirmed the diagnostic relevance of FOXM1, showing upregulated mRNA expression across various stages and metastasis. The influence of FOXM1 on immune cells, particularly CD4+, CD8+, and B cells, was significant, as revealed by immunohistochemistry. Protein-protein interaction analysis through STRING and CYTOSCAPE identified genes closely linked to FOXM1 in CRC. KEGG pathway enrichment suggested FOXM1's involvement in the p53 pathway, reinforcing its role in oncogenesis. Experimental validation confirmed elevated FOXM1 expression in HCT-116 and HT-29 cells. In summary, this study indicates that targeting FOXM1 could be a promising therapeutic strategy in CRC, emphasizing its importance in the molecular landscape of cancer progression.

Identification, prioritization, and evaluation of RlpA protein as a target against multidrug-resistant Pseudomonas aeruginosa.

According to the World Health Organization, infectious diseases, particularly those caused by multidrug-resistant bacteria (MDR), are projected to claim the lives of 15 million people by 2050. Septicemia carries a higher morbidity and mortality rate than infections caused by susceptible Pseudomonas aeruginosa, and MDR-mediated ocular infections can lead to impaired vision and blindness. To identify and develop a potential drug against MDR P. aeruginosa, we employed in silico reverse genetics-based target mining, drug prioritization, and evaluation. Rare Lipoprotein A (RlpA) was selected as the target protein, and its crystal structure was geometrically optimized. Molecular docking and virtual screening analyses revealed that RlpA exhibits strong binding affinity with 11 compounds. Among these, 3-chlorophthalic acid was evaluated, and subsequent in vitro assays demonstrated significant anti-Pseudomonas activity with negligible cytotoxicity. The compound was further evaluated against both drug-susceptible and MDR P. aeruginosa strains in vitro, with cytotoxicity assessed using an MTT assay. The study demonstrated that 3-chlorophthalic acid exhibits potent anti-Pseudomonas activity with minimal toxicity to host cells. Consequently, this compound emerges as a promising candidate against MDR P. aeruginosa, warranting further investigation.

Unveiling the ocular battlefield: Insights into Pseudomonas aeruginosa virulence factors and their implications for multidrug resistance.

The research investigates the virulence factors of Pseudomonas aeruginosa (P. aeruginosa), a pathogen known for its ability to cause human infections by releasing various exoenzymes and virulence factors. Particularly relevant in ocular infections, where tissue degeneration can occur, even after bacterial growth has ceased due to the potential role of secreted proteins/enzymes. Clinical isolates of P. aeruginosa, both ocular (146) and non-ocular (54), were examined to determine the frequency and mechanism of virulence factors. Phenotypic characterization revealed the production of alginate, biofilm, phospholipase C, and alkaline protease, while genotypic testing using internal uniplex PCR identified the presence of Exo U, S, T, Y, and LasB genes. Results showed a significant prevalence of Exo U and Y genes in ocular isolates, a finding unique to Indian studies. Additionally, the study noted that ocular isolates often contained all four secretomes, suggesting a potential link between these factors and ocular infections. These findings contribute to understanding the pathogenesis of P. aeruginosa infections, particularly in ocular contexts, and highlights the importance of comprehensive virulence factor analysis in clinical settings.

Identifying the molecular mechanisms of action of wound healing properties of Mathan tailam and Mahamegarajanga tailam in Wistar albino rats: Evidence through IL-10/VEGF/TNF-α signalling pathways.

The Siddha system of medicine (SSM) is the oldest medical science practised in the ancient period of the southern part of India and Sri Lanka. Many formulations were described for wound healing in the SSM, with specific diagnostic differentiation in the Siddha literature. Most preparations for wound healing were available in the form of oil-based formulations, especially for external usage. Mathan tailam (MT) and Mahamegarajanga tailam (MMRT) have been used by Siddha physicians and traditional practitioners to treat wounds. Mathan tailam is a popular regimen for skin lacerations, burns, skin infections, diabetic wounds, and dermatitis. Mahamegarajanga tailam has long been used by traditional vaidyars to treat cuts and burns. Both MT and MMRT are clinically well-appreciated drugs for wound healing and need to be studied for their mechanisms of action for scientific documentation. In an in vivo study on albino rats -excisional wound model, the histopathological changes, histo-immune response, biomarker analysis, and mRNA expression were studied and analysed. Wounds treated with MT and MMRT healed faster (p < 0.05) than the untreated group (CNT). Histological investigation showed rapid re-epithelialization, dense collagen deposition, increased enzymatic antioxidant activities and decreased lipid peroxidation in the MT and MMRT groups. mRNA expression reveals MT and MMRT-treated tissues able to induce convergent cell motility in wound space. Our study for the first time provides strong in vivo experimental evidence that Mathan tailam and Mahamegarajanga tailam play a crucial role in promoting skin tissue wound healing through IL-6/VEGF/TNF-α mediated mechanisms. Traditional practices continue to teach us valuable lessons, as seen by their continuous use in their locality for years.

Molecular analysis to identify novel potential biomarkers as drug targets in colorectal cancer therapy: an integrated bioinformatics analysis.

Colorectal cancer (CRC) is a heterogeneous disease that requires new diagnostic and prognostic markers. Integrated bioinformatics approach to identify novel therapeutic targets associated with CRC. Using GEO2R identified DEGs in CRC, and Funrich software facilitated the visualization of DEGs through Venn diagrams. From a total of 114 enhanced DEGs, potential hub genes were further filtered based on their nodal strength and edges using STRING database. To gain insights into the functional roles of these hub genes, gene ontology and pathway enrichment were conducted thorough g: profiler web server. Subsequently, overall survival plots from GEPIA and oncogenic predictive functions like mRNA expressions for stages and nodal metastasis were employed to identify hub genes in CRC patient samples. Additionally, the cBioPortal and HPA databases also revealed genetic alterations and expression levels in these hub genes in CRC patients, further supporting their involvement in colorectal cancer. Gene expression by RT-PCR shows upregulation of hub genes in HT-29 cells. Finally, our integrated bioinformatic analysis revealed that ABCE1, AURKA, HSPD1, PHKA1, CDK4, and YWHAE as hub genes with potential oncogenic roles in CRC. These genes hold promise as diagnostic and prognostic markers for colorectal tumorigenesis, providing insights into targeted therapies for improved patient outcomes.

Effect of Prunetin on Streptozotocin-Induced Diabetic Nephropathy in Rats - a Biochemical and Molecular Approach.

In the modern era, chronic kidney failure due to diabetes has spread across the globe. Prunetin (PRU), a component of herbal medicines, has a broad variety of pharmacological activities; these may help to slow the onset of diabetic kidney disease. The anti-nephropathic effects of PRU have not yet been reported. The present study explored the potential nephroprotective actions of PRU in diabetic rats. For 28 days, nephropathic rats were given oral doses of PRU (20, 40, and 80 mg/kg). Body weight, blood urea, creatinine, total protein, lipid profile, liver marker enzymes, carbohydrate metabolic enzymes, C-reactive protein, antioxidants, lipid peroxidative indicators, and the expression of insulin receptor substrate 1 (IRS-1) and glucose transporter 2 (GLUT-2) mRNA genes were all examined. Histological examinations of the kidneys, liver, and pancreas were also performed. The oral treatment of PRU drastically lowered the blood glucose, HbA1c, blood urea, creatinine, serum glutamic-oxaloacetic transaminase, serum glutamic pyruvic transaminase, alkaline phosphatase, lipid profile, and hexokinase. Meanwhile, the levels of fructose 1,6-bisphosphatase, glucose-6-phosphatase, and phosphoenol pyruvate carboxykinase were all elevated, but glucose-6-phosphate dehydrogenase dropped significantly. Inflammatory marker antioxidants and lipid peroxidative markers were also less persistent due to this administration. PRU upregulated the IRS-1 and GLUT-2 gene expression in the nephropathic group. The possible renoprotective properties of PRU were validated by histopathology of the liver, kidney, and pancreatic tissues. It is therefore proposed that PRU (80 mg/kg) has considerable renoprotective benefits in diabetic nephropathy in rats.

Piperine modulates IR/Akt/GLUT4 pathways to mitigate insulin resistance: Evidence from animal and computational studies.

The global prevalence of diabetes mellitus is rising, especially in India. Medicinal herbs, whether used alone or in combination with conventional medicines, have shown promise in managing diabetes and improving overall well-being. Piperine (PIP), a major bioactive compound found in pepper, is gaining attention for its beneficial properties. This study aimed to assess whether PIP could alleviate diabetes by targeting insulin pathway-related molecules in the adipose tissue of rats on a high-fat diet (HFD). After 60 days on the HFD, rats received PIP at a dose of 40 mg/kg body weight for one month. The results showed that PIP significantly improved metabolic indicators, antioxidant enzymes, and carbohydrate metabolic enzymes. It also regulated the mRNA and protein expression of insulin signaling, which had been disrupted by the diet and sucrose intake. Molecular docking analysis also revealed strong binding of PIP to key diabetes-related regulatory proteins, including Akt (-6.2 kcal/mol), IR (-7.02 kcal/mol), IRS-1 (-6.86 kcal/mol), GLUT4 (-6.24 kcal/mol), AS160 (-6.28 kcal/mol), and ß-arrestin (-6.01 kcal/mol). Hence, PIP may influence the regulation of glucose metabolism through effective interactions with these proteins, thereby controlling blood sugar levels due to its potent antilipidemic and antioxidant properties. In conclusion, our study provides in vivo experimental evidence against the HFD-induced T2DM model for the first time, making PIP a potential natural remedy to enhance the quality of life for diabetic patients and aid in their management.

Deregulation of apoptotic proteins by induction of Dendropthae falcata (L.f.) Ettingsh plant extract in breast cancer cells: A proteome-wide analysis.

Objectives: The present study evaluated the protein-based analysis to unravel the role and mechanism behind the Dendropthae falcata plant extract treatment in breast cancer cells. Materials and Methods: The protein sample was extracted from the cancer cells after treatment with the plant extract and subjected to two-dimensional electrophoresis for protein separation. Further, the proteins that were differentially regulated among the samples which were treated and non-treated were selected and processed further for protein identification using a tandem mass spectrometry approach. Results: Using these strategies, we identified 16 potential candidates which were showing remarkable changes in treated samples. All the candidates were analyzed further for gene ontology analysis, and it was observed that all proteins were involved in multiple pathways pertaining to the carcinogenesis process. Specifically, apoptotic pathway proteins including BAD, BIK, BID, CASP8, MCL1, BCL2, and BAK1 were highly impacted by treatment with D. falcata plant extract. All these protein hits were further taken for validation experiments using RT PCR analysis. Conclusion: Initiation of these apoptotic proteins by D. falcata plant extract treatment in breast cancer cells shows a positive direction toward nature-based alternative medicine.

Glyphosate potentiates insulin resistance in skeletal muscle through the modulation of IRS-1/PI3K/Akt mediated mechanisms: An in vivo and in silico analysis.

Herbicides have been linked to a higher risk of developing diabetes. Certain herbicides also operate as environmental toxins. Glyphosate is a popular and extremely effective herbicide for weed control in grain crops that inhibits the shikimate pathway. It has been shown to negatively influence endocrine function. Few studies have demonstrated that glyphosate exposure results in hyperglycemic and insulin resistance; but the molecular mechanism underlying the diabetogenic potential of glyphosate on skeletal muscle, a primary organ that includes insulin-mediated glucose disposal, is unknown. In this study, we aimed to evaluate the impact of glyphosate on the detrimental changes in the insulin metabolic signaling in the gastrocnemius muscle. In vivo results showed that glyphosate exposure caused hyperglycemia, dyslipidemia, increased glycosylated hemoglobin (HbA1c), liver function, kidney function profile, and oxidative stress markers in a dose-dependent fashion. Conversely, hemoglobin and antioxidant enzymes were significantly reduced in glyphosate-induced animals indicating its toxicity is linked to induce insulin resistance. The histopathology of the gastrocnemius muscle and RT-PCR analysis of insulin signaling molecules revealed glyphosate-induced alteration in the expression of IR, IRS-1, PI3K, Akt, ß-arrestin-2, and GLUT4 mRNA. Lastly, molecular docking and dynamics simulations confirmed that glyphosate showed a high binding affinity with target molecules such as Akt, IRS-1, c-Src, ß-arrestin-2, PI3K, and GLUT4. The current work provides experimental proof that glyphosate exposure has a deleterious effect on the IRS-1/PI3K/Akt signaling pathways, which in turn causes the skeletal muscle to become insulin resistant and eventually develop type 2 diabetes mellitus.

An Update on the Effectiveness of Probiotics in the Prevention and Treatment of Cancer.

Probiotics are living microbes that play a significant role in protecting the host in various ways. Gut microbiota is one of the key players in maintaining homeostasis. Cancer is considered one of the most significant causes of death worldwide. Although cancer treatment has received much attention in recent years, the number of people suffering from neoplastic syndrome continues to increase. Despite notable improvements in the field of cancer therapy, tackling cancer has been challenging due to the multiple properties of cancer cells and their ability to evade the immune system. Probiotics alter the immunological and cellular responses by enhancing the epithelial barrier and stimulating the production of anti-inflammatory, antioxidant, and anticarcinogenic compounds, thereby reducing cancer burden and growth. The present review focuses on the various mechanisms underlying the role of probiotics in the prevention and treatment of cancer.

Impact of Glyphosate on the Development of Insulin Resistance in Experimental Diabetic Rats: Role of NFκB Signalling Pathways.

Glyphosate, an endocrine disruptor, has an adverse impact on human health through food and also has the potential to produce reactive oxygen species (ROS), which can lead to metabolic diseases. Glyphosate consumption from food has been shown to have a substantial part in insulin resistance, making it a severe concern to those with type 2 diabetes (T2DM). However, minimal evidence exists on how glyphosate impacts insulin-mediated glucose oxidation in the liver. Hence the current study was performed to explore the potential of glyphosate toxicity on insulin signaling in the liver of experimental animals. For 16 weeks, male albino Wistar rats were given 50 mg, 100 mg and 250 mg/kg b. wt. of glyphosate orally. In the current study, glyphosate exposure group was linked to a rise in fasting sugar and insulin as well as a drop in serum testosterone. At the same time, in a dose dependent fashion, glyphosate exposure showed alternations in glucose metabolic enzymes. Glyphosate exposure resulted in a raise in H2O2 formation, LPO and a reduction in antioxidant levels those results in impact on membrane integrity and insulin receptor efficacy in the liver. It also registered a reduced levels of mRNA and protein expression of insulin receptor (IR), glucose transporter-2 (GLUT2) with concomitant increase in the production of proinflammatory factors such as JNK, IKKß, NFkB, IL-6, IL-1ß, and TNF-α as well as transcriptional factors like SREBP1c and PPAR-γ leading to pro-inflammation and cirrhosis in the liver which results in the development of insulin resistance and type 2 diabetes. Our present findings for the first time providing an evidence that exposure of glyphosate develops insulin resistance and type 2 diabetes by aggravating NFkB signaling pathway in liver.

Antimicrobial activity of polyphenolic compounds from Spirulina against food-borne bacterial pathogens.

Food-borne drug-resistant bacteria have adverse impacts on both food manufacturers and consumers. Disillusionment with the efficacy of current preservatives and antibiotics for controlling food-borne pathogens, especially drug-resistant bacteria, has led to a search for safer alternatives from natural sources. Spirulina have been recognized as a food supplement, natural colorant, and enriched source of bioactive secondary metabolites. The main objectives of this study were to isolate polyphenolic compounds from Spirulina and analyze their antibacterial potential against drug-resistant food-borne bacterial pathogens. We found that fraction B of methanol extract contained a high quantity of polyphenols exhibiting broad spectrum antimicrobial effects against drug-resistant food-borne bacterial pathogens. Potential secondary metabolites, such as benzophenone, dihydro-methyl-phenylacridine, carbanilic acid, dinitrobenzoate, propanediamine, isoquinoline, piperidin, oxazolidin, and pyrrolidine, were identified by gas chromatography and mass spectrophotometry (GCMS). These metabolites are active against both gram-positive and gram-negative pathogens. Our work suggests that phenolic compounds from Spirulina provide a natural and sustainable source of food preservatives for future use.

Antifungal activity of nanoemulsion from Cleome viscosa essential oil against food-borne pathogenic Candida albicans.

Pathogenic and spoilage fungi cause enormous challenges to food related fatal infections. Plant essential oil based classical emulsions can functions as antifungal agents. To investigate the antifungal spectrum, that is the scope of the nanoemulsion composed of Cleome viscosa essential oil and Triton-x-100 fabricated by ultrasonication method. Minimum inhibitory and fungicidal concentration of essential oil nanoemulsion (EONE) was tested against food borne pathogenic C. albicans. The MIC and MFC values ranged from 16.5 to 33 µl/ml with significant reduction on biofilm of C. albicans isolates. The alteration of molecular fingerprints was confirmed by Fourier transformed infrared spectroscopy and subsequent reduction of chitin levels in cell walls was noted by spectroscopic analysis. The EONE and their bioactive compounds cause collateral damage on C. albicans cells.

Architectural and Ultrastructural Variations of Human Leukocyte-Rich Platelet-Rich Fibrin and Injectable Platelet-Rich Fibrin.

BACKGROUND: Platelet-rich fibrin (PRF) architecture and ultrastructure plays a crucial role in regulating and coordinating the cellular functions and provides a physical architecture, mechanical stability, and biochemical cues necessary for tissue morphogenesis and homeostasis. No study consciously reported the variation in architecture, ultrastructure, and morphology of leukocyte-rich PRF (L-PRF) and injectable PRF (i-PRF). OBJECTIVE: Hence, the present study was aimed to evaluate the fibrin architecture, ultrastructure, and cell contents of autologous L-PRF and i-PRF. MATERIALS AND METHODS: The autologous L-PRF and i-PRF were prepared from blood samples of healthy donors. The morphological and structural variations were assessed by histopathology, atomic force microscopy, confocal laser scanning microscope, and field emission scanning electron microscope. RESULTS: Disparity was found on architecture and ultrastructure of L-PRF and i-PRF fibrin network. The variation in platelet and leukocyte concentration attributed to the fibrin conformational changes. L-PRF shows thick fibrins with rough surface, whereas in i-PRF, smooth thin fibrins. CONCLUSIONS: The current study revealed that there is heterogeneity between L-PRF and i-PRF fibrin matrix architecture, ultrastructure, platelets, leukocytes, and the fibrin content. These speculate that the diameter, width, roughness, and smoothness of fibrin fibers, pore size, and shapes of L-PRF and i-PRF matrix may initiate and mediate the scaffold functions differently.

Cytokine Expression Pattern and Protein-Protein interaction network analysis of Leucocyte Rich Platelet Rich Fibrin and Injectable Form of Platelet Rich Fibrin.

PURPOSE: Platelet-rich fibrin (PRF) such as leucocyte-rich PRF (L-PRF) and injectable form of PRF (i-PRF) are widely used in various surgical applications. L-PRF- and i-PRF-derived cytokine variations and functional pathways are still unexplored. The aim of the study was to evaluate the expression pattern of Th1-, Th2-, and Th17-related cytokines by L-PRF and i-PRF under in vitro. METHODS: Cytokine levels were evaluated using multi-analyte ELISArray kit. Using elevated level of cytokines, the protein-protein interaction and pathway were predicted by computational method. RESULTS: The expressed cytokine levels were higher in L-PRF than in i-PRF. Specifically in L-PRF, IL8, IL2, IL6, and IL1A were expressed abundantly, whereas IL4, IL10, and IL6 were significantly high in i-PRF. Furthermore, protein-protein interaction (PPI) networks (cytokine-cytokine interactions) and pathway analyses were predicted using higher-order cytokines. PPI networks and gene ontology enrichment analysis showed functional variations between L-PRF and i-PRF. Kyoto Encyclopedia of Gene and Genome pathway analysis found that L-PRF mediates NF-k B signaling, Toll-like receptor signaling (TLR), and MAPK signaling via T-cell receptor signaling pathway. i-PRF is significantly involved in JAK-STAT signaling pathway through upregulation of STAT1. CONCLUSION: Our study concludes that L-PRF and i-PRF act via different pathways that confirm functional variations between them. Therefore, we speculate that L-PRF may be effective in acute phase of chronic wounds such as in diabetes mellitus and immunocompromised patients whereas i-PRF may have a better outcome in acute wounds.