Gut instinct: harnessing the power of probiotics to tame pathogenic signaling pathways in ulcerative colitis.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) marked by persistent inflammation of the mucosal lining of the large intestine, leading to debilitating symptoms and reduced quality of life. Emerging evidence suggests that an imbalance of the gut microbiota plays a crucial role in UC pathogenesis, and various signaling pathways are implicated in the dysregulated immune response. Probiotics are live microorganisms that confer health benefits to the host, have attracted significant attention for their potential to restore gut microbial balance and ameliorate inflammation in UC. Recent studies have elucidated the mechanisms by which probiotics modulate these signaling pathways, often by producing anti-inflammatory molecules and promoting regulatory immune cell function. For example, probiotics can inhibit the nuclear factor-κB (NF-κB) pathway by stabilizing Inhibitor of kappa B alpha (IκBα), dampening the production of proinflammatory cytokines. Similarly, probiotics can modulate the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway, suppressing the activation of STAT1 and STAT3 and thus reducing the inflammatory response. A better understanding of the underlying mechanisms of probiotics in modulating pathogenic signaling pathways in UC will pave the way for developing more effective probiotic-based therapies. In this review, we explore the mechanistic role of probiotics in the attenuation of pathogenic signaling pathways, including NF-κB, JAK/STAT, mitogen-activated protein kinases (MAPKs), Wnt/ß-catenin, the nucleotide-binding domain (NOD)-, leucine-rich repeat (LRR)- and pyrin domain-containing protein 3 (NLRP3) inflammasome, Toll-like receptors (TLRs), interleukin-23 (IL-23)/IL-17 signaling pathway in UC.

Reducing metastasis ability of gastric cancer cell line by targeting MMP16 using miR-193a-5p and 5-FU.

PURPOSE: Co-administration of microRNAs and chemotherapy drugs effectively treats several cancers. The current study sought to investigate the function of matrix metalloproteinase 16 (MMP16) and miR-193a-5p in the pathogenesis of gastric cancer (GC). MATERIALS/METHODS: Sixty-five surgical patients, 15 receiving 5-fluorouracil (5-FU), provided GC and adjacent non-cancerous tissue. Following that, qPCR was used to assess the expression levels of MMP16 and miR-193a-5p in GC cells. The impact of miR-193a-5p and 5-FU administration on MMP16 mRNA expression was evaluated using qRT-PCR and Western blotting. MTT and Scratch tests were also conducted to assess their effects on cell viability and migration. Moreover, a rescue experiment using an MTT assay was performed. Using flow cytometry, the apoptotic rate was calculated. Finally, it was evaluated how MMP16 and miR-193a-5p related to the clinicopathological characteristics of the patients. RESULTS: The current study found that while MMP16 expression increased in GC patients (P<0.0001), miR-193a-5p expression significantly decreased (P<0.001). MMP16 down-regulation was another effect of miR-193a-5p replacement, particularly when 5-FU was added (P<0.01). In addition, this study found that miR-193a-5p, by concentrating on MMP16, decreased the migration of GC cells brought on by MMP16. In GC cell lines, miR-193 and 5-FU induce apoptosis, with the 5-FU being more pronounced when combined with mir-193, according to flow cytometry results. A strong correlation was also found between clinicopathological traits associated with MMP16 and miR-193a-5p. CONCLUSIONS: These findings suggest that miR-193a-5p, in conjunction with 5-FU, down-regulates MMP16 in GC, where it suppresses tumor growth.

Identification of potential inhibitors against Corynebacterium diphtheriae MtrA response regulator protein; an in-silico drug discovery approach.

Corynebacterium diphtheriae is a multi-drug resistant bacteria responsible for the life-threatening respiratory illness, diphtheria which can lead to severe Nervous system disorders, mainly infecting the lungs, heart, and kidneys if left untreated. In the current study, Corynebacterium diphtheriae MtrA response regulator protein was targeted, which regulates a two-component system of bacterial pathogenesis, and initiates DNA replication and cell division. In the current study a computational approach have been described for drug development against C. diphtheriae infections by inhibiting MtrA protein by small molecules acting as potential inhibitors against it. Molecular docking analysis of the equilibrated MtrA protein revealed compound-0.2970, compound-0.3029, and compound-0.3016 from Asinex Library as the promising inhibitors based on their lowest binding energies (-9.8 kJ/mol, -9.2 kJ/mol, and -8.9 kJ/mol), highest gold scores (40.53, 47.41, and 48.41), drug-likeness and pharmacokinetic properties. The MD simulation studies of the identified top-ranked inhibitors at 100 ns elucidated the system stability and fluctuations in the binding pocket of MtrA protein. Molecular Dynamics Simulations of the top three docked complexes further revealed that the standard binding pocket was retained ensuring the system stability. The rearrangements of H-bonds, van der Waals, pi-pi, and solid hydrophobic interactions were also observed. The binding free energy calculations (MM/PBSA and MM/GBSA) suggested a fundamental binding capability of the ligand to the target receptor MtrA. Therefore, the current study has provided excellent candidates acting as potent inhibitors for developing therapeutic drugs against C. diphtheriae infections. However, in vivo and in vitro animal experiments and accurate clinical trials are needed to validate the potential inhibitory effect of these compounds.

The effects of selenium supplementation on lipid profile in adults: A systematic review and meta-analysis of randomized controlled trials.

INTRODUCTION: Dyslipidemia with a considerable progression rate is a primary risk factor for CVDs if left untreated. Dietary interventions have explored the health influences of selenium on lipid profiles in adults, yet the findings remain contentious. This study seeks to determine if selenium supplementation can positively modify the lipid profile (total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL), and high-density lipoprotein cholesterol (HDL-C) in adults. METHODS: Using predefined keywords, we searched online databases, including Scopus, PubMed, Web of Science Core Collection, and Google Scholar, for relevant studies published from inception through July 2024. A random-effects meta-analysis was then employed to pool the weighted mean differences (WMD) and 95 % CI for outcomes assessed by a minimum of three studies. RESULTS: Initially 1205 studies were obtained out of which 25 RCTs were decided to be included for further analyses. Selenium supplementation reduced VLDL (WMD: -1.53; 95 % CI: -2.86, -0.20), but did not change TG (WMD: 1.12; 95 % CI: -4.51, 6.74), TC (WMD: -2.25; 95 % CI: -6.80, 2.29), LDL-C (WMD: 1.60; 95 % CI: -4.26, 7.46), and HDL-C levels (WMD: 0.98; 95 % CI: - 0.02, 1.98). CONCLUSION: Our study showed significantly reduced VLDL but limited effects were observed in other lipid indexes. More extensive RCTs are required globally to achieve a holistic comprehension of the connection between selenium and lipid profile.

Role of circRNAs in regulating cell death in cancer: a comprehensive review.

Despite multiple diagnostic and therapeutic advances, including surgery, radiation therapy, and chemotherapy, cancer preserved its spot as a global health concern. Prompt cancer diagnosis, treatment, and prognosis depend on the discovery of new biomarkers and therapeutic strategies. Circular RNAs (circRNAs) are considered as a stable, conserved, abundant, and varied group of RNA molecules that perform multiple roles such as gene regulation. There is evidence that circRNAs interact with RNA-binding proteins, especially capturing miRNAs. An extensive amount of research has presented the substantial contribution of circRNAs in various types of cancer. To fully understand the linkage between circRNAs and cancer growth as a consequence of various cell death processes, including autophagy, ferroptosis, and apoptosis, more research is necessary. The expression of circRNAs could be controlled to limit the occurrence and growth of cancer, providing a more encouraging method of cancer treatment. Consequently, it is critical to understand how circRNAs affect various forms of cancer cell death and evaluate whether circRNAs could be used as targets to induce tumor death and increase the efficacy of chemotherapy. The current study aims to review and comprehend the effects that circular RNAs exert on cell apoptosis, autophagy, and ferroptosis in cancer to investigate potential cancer treatment targets.

The role of gut-derived short-chain fatty acids in Parkinson's disease.

The emerging function of short-chain fatty acids (SCFAs) in Parkinson's disease (PD) has been investigated in this article. SCFAs, which are generated via the fermentation of dietary fiber by gut microbiota, have been associated with dysfunction of the gut-brain axis and, neuroinflammation. These processes are integral to the development of PD. This article examines the potential therapeutic implications of SCFAs in the management of PD, encompassing their capacity to modulate gastrointestinal permeability, neuroinflammation, and neuronal survival, by conducting an extensive literature review. As a whole, this article emphasizes the potential therapeutic utility of SCFAs as targets for the management and treatment of PD.

Association of polyomavirus infection with lung cancer: A systematic review and meta-analysis.

AIM: The objective of this study was to investigate the pooled prevalence and possible association between polyomavirus infection and lung cancer. METHODS: A systematic publication search was conducted by identifying relevant cross-sectional and case-control studies from major online databases. Heterogeneity, OR, and corresponding 95 % CI were applied to all studies through meta-analysis and forest plot. Random effects models were used to calculate the overall pooled prevalence. Visual inspection of a funnel plot plotting the log-transformed OR and its associated standard error of the log (OR) was combined with the Begg and Egger test to examine the presence and influence of publication bias. Analyzes were performed using Stata software v.14.1. RESULTS: 23 articles (33 datasets) were included in the meta-analysis, of which 14 datasets were case/control and the rest were cross-sectional studies. The pooled polyomavirus infection rate in lung cancer patients was 0.06 % (0.02-0.11 %). In subgroup analysis, the pooled prevalence of JCV, MCPyV, KI, SV40, BKV, WU, MU, and STL was 21 %, 7 %, 6 %, 2 %, 0 %, 0 %, 0 %, and 0 % respectively. An association has been found between polyomavirus infection and lung cancer [summary OR 6.33 (95 % CI (1.76-22.77); I2=67.45 %)]. The subgroup analysis, based on the virus type, showed a strong association between MCPyV and lung cancer [summary OR 13.61 (95 % CI 2.41-76.59; I2=40.0 %)]. despite the high prevalence of JCV DNA in lung cancer tissue, analysis of case-control studies showed that JCV is not associated with lung cancer and does not increase the risk of lung cancer. CONCLUSION: This study showed a significant association between polyomaviruses infection with lung cancer. The results also revealed a pooled prevalence of 6 % for polyomaviruses in lung tumor patients. Altogether, the findings of the present work suggest that Merkel cell polyomavirus infection is a potential risk factor for lung cancer.

MicroRNAs Modulating Neuroinflammation in Parkinson's disease.

Parkinson's disease (PD) is one of the most frequent age-associated neurodegenerative disorder. Presence of α-synuclein-containing aggregates in the substantia nigra pars compacta (SNpc) and loss of dopaminergic (DA) neurons are among the characteristic of PD. One of the hallmarks of PD pathophysiology is chronic neuroinflammation. Activation of glial cells and elevated levels of pro-inflammatory factors are confirmed as frequent features of the PD brain. Chronic secretion of pro-inflammatory cytokines by activated astrocytes and microglia exacerbates DA neuron degeneration in the SNpc. MicroRNAs (miRNAs) are among endogenous non-coding small RNA with the ability to perform post-transcriptional regulation in target genes. In that regard, the capability of miRNAs for modulating inflammatory signaling is the center of attention in many investigations. MiRNAs could enhance or limit inflammatory signaling, exacerbating or ameliorating the pathological consequences of extreme neuroinflammation. This review summarizes the importance of inflammation in the pathophysiology of PD. Besides, we discuss the role of miRNAs in promoting or protecting neural cell injury in the PD model by controlling the inflammatory pathway. Modifying the neuroinflammation by miRNAs could be considered a primary therapeutic strategy for PD.

Small molecule and big function: MicroRNA-mediated apoptosis in rheumatoid arthritis.

Rheumatoid arthritis (RA) is a common autoimmune condition and chronic inflammatory disease, mostly affecting synovial joints. The complex pathogenesis of RA is supportive of high morbidity, disability, and mortality rates. Pathological changes a common characteristic in RA synovial tissue is attributed to the inadequacy of apoptotic pathways. In that regard, apoptotic pathways have been the center of attention in RA therapeutic approaches. As the regulators in the complex network of apoptosis, microRNAs (miRNAs) are found to be vital modulators in both intrinsic and extrinsic pathways through altering their regulatory genes. Indeed, miRNA, a member of the family of non-coding RNAs, are found to be an important player in not even apoptosis, but proliferation, gene expression, signaling pathways, and angiogenesis. Aberrant expression of miRNAs is implicated in attenuation and/or intensification of various apoptosis routes, resulting in culmination of human diseases including RA. Considering the need for more studies focused on the underlying mechanisms of RA in order to elevate the unsatisfactory clinical treatments, this study is aimed to delineate the importance of apoptosis in the pathophysiology of this disease. As well, this review is focused on the critical role of miRNAs in inducing or inhibiting apoptosis of RA-synovial fibroblasts and fibroblast-like synoviocytes and how this mechanism can be exerted for therapeutic purposes for RA.

MicroRNA as Key Players in Hepatocellular Carcinoma: Insights into Their Role in Metastasis.

Liver cancer or hepatocellular carcinoma (HCC) remains the most common cancer in global epidemiology. Both the frequency and fatality of this malignancy have shown an upward trend over recent decades. Liver cancer is a significant concern due to its propensity for both intrahepatic and extrahepatic metastasis. Liver cancer metastasis is a multifaceted process characterized by cell detachment from the bulk tumor, modulation of cellular motility and invasiveness, enhanced proliferation, avoidance of the immune system, and spread either via lymphatic or blood vessels. MicroRNAs (miRNAs) are small non-coding ribonucleic acids (RNAs) playing a crucial function in the intricate mechanisms of tumor metastasis. A number of miRNAs can either increase or reduce metastasis via several mechanisms, such as control of motility, proliferation, attack by the immune system, cancer stem cell properties, altering the microenvironment, and the epithelial-mesenchymal transition (EMT). Besides, two other types of non-coding RNAs, such as long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) can competitively bind to endogenous miRNAs. This competition results in the impaired ability of the miRNAs to inhibit the expression of the specific messenger RNAs (mRNAs) that are targeted. Increasing evidence has shown that the regulatory axis comprising circRNA/lncRNA-miRNA-mRNA is correlated with the regulation of HCC metastasis. This review seeks to present a thorough summary of recent research on miRNAs in HCC, and their roles in the cellular processes of EMT, invasion and migration, as well as the metastasis of malignant cells. Finally, we discuss the function of the lncRNA/circRNA-miRNA-mRNA network as a crucial modulator of carcinogenesis and the regulation of signaling pathways or genes that are relevant to the metastasis of HCC. These findings have the potential to offer valuable insight into the discovery of novel therapeutic approaches for management of liver cancer metastasis.

Epithelial-mesenchymal transition in chemoradiation-induced lung damage: Mechanisms and potential treatment approaches.

Pulmonary injury is one of the key restricting factors for the therapy of malignancies with chemotherapy or following radiotherapy for chest cancers. The lung is a sensitive organ to some severely toxic antitumor drugs, consisting of bleomycin and alkylating agents. Furthermore, treatment with radiotherapy may drive acute and late adverse impacts on the lung. The major consequences of radiotherapy and chemotherapy in the lung are pneumonitis and fibrosis. Pneumonitis may arise some months to a few years behind cancer therapy. However, fibrosis is a long-term effect that appears years after chemo/or radiotherapy. Several mechanisms such as oxidative stress and severe immune reactions are implicated in the progression of pulmonary fibrosis. Epithelial-mesenchymal transition (EMT) is offered as a pivotal mechanism for lung fibrosis behind chemotherapy and radiotherapy. It seems that pulmonary fibrosis is the main consequence of EMT after chemo/radiotherapy. Several biological processes, consisting of the liberation of pro-inflammatory and pro-fibrosis molecules, oxidative stress, upregulation of nuclear factor of κB and Akt, epigenetic changes, and some others, may participate in EMT and pulmonary fibrosis behind cancer therapy. In this review, we aim to discuss how chemotherapy or radiotherapy may promote EMT and lung fibrosis. Furthermore, we review potential targets and effective agents to suppress EMT and lung fibrosis after cancer therapy.

Targeting the pancreatic tumor microenvironment by plant-derived products and their nanoformulations.

Pancreatic cancer remains a significant health issue with limited treatment options. The tumor stroma, a complex environment made up of different cells and proteins, plays a crucial role in tumor growth and chemoresistance. Targeting tumor stroma, consisting of diverse non-tumor cells such as fibroblasts, extracellular matrix (ECM), immune cells, and also pre-vascular cells is encouraging for remodeling solid cancers, such as pancreatic cancer. Remodeling the stroma of pancreas tumors can be suggested as a strategy for reducing resistance to chemo/immunotherapy. Several studies have shown that phytochemicals from plants can affect the tumor environment and have anti-cancer properties. By targeting key pathways involved in stromal activation, phytochemicals may disrupt communication between the tumor and stroma and make tumor cells more sensitive to different treatments. Additionally, phytochemicals have immunomodulatory and anti-angiogenic properties, all of which contribute to their potential in treating pancreatic cancer. This review will provide a detailed look at how phytochemicals impact the tumor stroma and their effects on pancreatic tumor growth, spread, and response to treatment. It will also explore the potential of combining phytochemicals with other treatment options like chemotherapy, immunotherapy, and radiation.

Detailed role of SR-A1 and SR-E3 in tumor biology, progression, and therapy.

The first host defense systems are the innate immune response and the inflammatory response. Among innate immune cells, macrophages, are crucial because they preserve tissue homeostasis and eradicate infections by phagocytosis, or the ingestion of particles. Macrophages exhibit phenotypic variability contingent on their stimulation state and tissue environment and may be detected in several tissues. Meanwhile, critical inflammatory functions are played by macrophage scavenger receptors, in particular, SR-A1 (CD204) and SR-E3 (CD206), in a variety of pathophysiologic events. Such receptors, which are mainly found on the surface of multiple types of macrophages, have different effects on processes, including atherosclerosis, innate and adaptive immunity, liver and lung diseases, and, more recently, cancer. Although macrophage scavenger receptors have been demonstrated to be active across the disease spectrum, conflicting experimental findings and insufficient signaling pathways have hindered our comprehension of the molecular processes underlying its array of roles. Herein, as SR-A1 and SR-E3 functions are often binary, either protecting the host or impairing the pathophysiology of cancers has been reviewed. We will look into their function in malignancies, with an emphasis on their recently discovered function in macrophages and the possible therapeutic benefits of SR-A1 and SR-E3 targeting.

Advances in chitosan-based blends as potential drug delivery systems: A review.

During the last decades, the ever-increasing incidence of diseases has led to high rates of mortality throughout the world. On the other hand, the inability and deficiencies of conventional approaches (such as chemotherapy) in the suppression of diseases remain challenging issues. As a result, there is a fundamental requirement to develop novel, biocompatible, bioavailable, and practical nanomaterials to prevent the incidence and mortality of diseases. Chitosan (CS) derivatives and their blends are outstandingly employed as promising drug delivery systems for disease therapy. These biopolymers are indicated more efficient performance against diseases compared with conventional modalities. The CS blends possess improved physicochemical properties, ease of preparation, high affordability, etc. characteristics compared with other biopolymers and even pure CS which result in efficient thermal, mechanical, biochemical, and biomedical features. Also, these blends can be administrated through different routes without a long-term treatment period. Due to the mentioned properties, numerous formulations of CS blends are developed for pharmaceutical sciences to treat diseases. This review article highlights the progressions in the development of CS-based blends as potential drug delivery systems against diseases.

Stealth Nanocarriers in Cancer Therapy: a Comprehensive Review of Design, Functionality, and Clinical Applications.

Nanotechnology has significantly transformed cancer treatment by introducing innovative methods for delivering drugs effectively. This literature review provided an in-depth analysis of the role of nanocarriers in cancer therapy, with a particular focus on the critical concept of the 'stealth effect.' The stealth effect refers to the ability of nanocarriers to evade the immune system and overcome physiological barriers. The review investigated the design and composition of various nanocarriers, such as liposomes, micelles, and inorganic nanoparticles, highlighting the importance of surface modifications and functionalization. The complex interaction between the immune system, opsonization, phagocytosis, and the protein corona was examined to understand the stealth effect. The review carefully evaluated strategies to enhance the stealth effect, including surface coating with polymers, biomimetic camouflage, and targeting ligands. The in vivo behavior of stealth nanocarriers and their impact on pharmacokinetics, biodistribution, and toxicity were also systematically examined. Additionally, the review presented clinical applications, case studies of approved nanocarrier-based cancer therapies, and emerging formulations in clinical trials. Future directions and obstacles in the field, such as advancements in nanocarrier engineering, personalized nanomedicine, regulatory considerations, and ethical implications, were discussed in detail. The review concluded by summarizing key findings and emphasizing the transformative potential of stealth nanocarriers in revolutionizing cancer therapy. This review enhanced the comprehension of nanocarrier-based cancer therapies and their potential impact by providing insights into advanced studies, clinical applications, and regulatory considerations.

Advancing therapeutic efficacy: nanovesicular delivery systems for medicinal plant-based therapeutics.

The utilization of medicinal plant extracts in therapeutics has been hindered by various challenges, including poor bioavailability and stability issues. Nanovesicular delivery systems have emerged as promising tools to overcome these limitations by enhancing the solubility, bioavailability, and targeted delivery of bioactive compounds from medicinal plants. This review explores the applications of nanovesicular delivery systems in antibacterial and anticancer therapeutics using medicinal plant extracts. We provide an overview of the bioactive compounds present in medicinal plants and their therapeutic properties, emphasizing the challenges associated with their utilization. Various types of nanovesicular delivery systems, including liposomes, niosomes, ethosomes, and solid lipid nanoparticles, among others, are discussed in detail, along with their potential applications in combating bacterial infections and cancer. The review highlights specific examples of antibacterial and anticancer activities demonstrated by these delivery systems against a range of pathogens and cancer types. Furthermore, we address the challenges and limitations associated with the scale-up, stability, toxicity, and regulatory considerations of nanovesicular delivery systems. Finally, future perspectives are outlined, focusing on emerging technologies, integration with personalized medicine, and potential collaborations to drive forward research in this field. Overall, this review underscores the potential of nanovesicular delivery systems for enhancing the therapeutic efficacy of medicinal plant extracts in antibacterial and anticancer applications, while identifying avenues for further research and development.

Photoacoustic imaging in prostate cancer: A new paradigm for diagnosis and management.

The global health issue of prostate cancer (PCa) requires better diagnosis and treatment. Photoacoustic imaging (PAI) may change PCa management. This review examines PAI's principles, diagnostic role, and therapeutic guidance. PAI uses optical light excitation and ultrasonic detection for high-resolution functional and molecular imaging. PAI uses endogenous and exogenous contrast agents to distinguish cancerous and benign prostate tissues with greater sensitivity and specificity than PSA testing and TRUS-guided biopsy. In addition to diagnosing, PAI can guide and monitor PCa therapy. Its real-time imaging allows precise biopsies and brachytherapy seed placement. Photoacoustic temperature imaging allows non-invasive monitoring of thermal therapies like cryotherapy, improving treatment precision and success. Transurethral illumination probes, innovative contrast agents, integration with other imaging modalities, and machine learning analysis are being developed to overcome depth and data complexity restrictions. PAI could become an essential tool for PCa diagnosis and therapeutic guidance as the field advances.

The role of Interleukin-21 (IL-21) in allergic disorders: Biological insights and regulatory mechanisms.

In recent decades, allergic diseases subsequent from an IgE-mediated response to specific allergens have become a progressively public chronic disease worldwide. They have shaped an important medical and socio-economic burden. A significant proportion of allergic disorders are branded via a form 2 immune response relating Th2 cells, type 2 natural lymphoid cells, mast cells and eosinophils. Interleukin-21 (IL-21) is a participant of the type-I cytokine family manufactured through numerous subsets of stimulated CD4+ T cells and uses controlling properties on a diversity of immune cells. Increasingly, experimental sign suggests a character for IL-21 in the pathogenesis of numerous allergic disorders. The purpose of this review is to discuss the biological properties of IL-21 and to summaries current developments in its role in the regulation of allergic disorders.

Assessing the gas sensing capability of undoped and doped aluminum nitride nanotubes.

CONTEXT: CO2 and CO gas sensors are very important to recognize the insulation situation of electrical tools. ToCO explore the application of noble metal doped of aluminum nitride nanotubes for gas sensors, DFT computations according to the first principal theory were applied to study sensitivity, adsorption attributes, and electronic manner. In this investigation, platinum-doped aluminum nitride nanotubes were offered for the first time to analyze the adsorption towards CO2 and CO gases. Firm construction of platinum-doped aluminum nitride nanotubes (Pt-AlNNT) was investigated in four feasible places, and the binding energy of firm construction is 1.314 eV. Respectively, the adsorption energy between the CO2 and Pt-AlNNT systems was - 2.107 eV, while for instance of CO, the adsorption energy was - 3.258 eV. The mentioned analysis and computations are considerable for studying Pt-AlNNT as a new CO2 and CO gas sensor for electrical tools insulation. The current study revealed that the Pt-AlNNT possesses high selectivity and sensitivity towards CO2 and CO. METHODS: In this research, Pt-doped AlNNT (Pt-AlNNT) has been studied as sensing materials of CO and CO2 for the first time. The adsorption process of Pt-AlNNT has been computed and analyzed through the DFT approach. DFT computations by using B3LYP functional and 6-31 + G* basis sets have been applied in the GAMESS code for sensing attributes, which contribute to potential applications.