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In recent years, people's living standards are getting higher and higher, and life pressure is also increasing, and there are also many problems in eating habits. This is also the direct cause of colon cancer. The aim of this paper was to investigate whether anesthetic drugs could positively affect the proliferation and apoptosis of colon cancer cells. In this paper, the significance of anesthetic drugs is proposed, and an artificial neural network algorithm based on artificial intelligence is proposed. It is well known that artificial neural networks play an important role in medicine. The experimental results of this paper show that the incidence of colon cancer in 2020 will be in the range of 5%-35%, and the incidence of colon cancer in 2021 will be in the range of 7%-30%. While colon cancer rates in 2021 do not appear to be as high as colon cancer rates in 2020, they are generally much higher than colon cancer rates in 2020. It can be seen that as the population ages, the number of colon cancer patients is increasing due to the lack of emphasis on health. This also means that the incidence of colon cancer is getting higher and higher, and traditional drug chemotherapy has been unable to play a good role in inhibiting the proliferation of colon cancer cells. Therefore, this paper investigated the effects of anesthetic drugs on the proliferation and apoptosis of human colon cancer cells. [ABSTRACT FROM AUTHOR]

Ferroptosis is a novel form of programmed cell death characterized by the accumulation of iron-dependent lipid peroxides, which causes membrane injury. Under the catalysis of iron ions, cells deficient in glutathione peroxidase (GPX4) cannot preserve the balance in lipid oxidative metabolism, and the buildup of reactive oxygen species on the membrane lipids leads to cell death. An increasing body of evidence suggests that ferroptosis plays a significant role in the development and occurrence of cardiovascular diseases. In this paper, we mainly elaborated on the molecular mechanisms regulating ferroptosis and its impact on cardiovascular disease to lay the groundwork for future studies on the prophylaxis and treatment of this patient population. [ABSTRACT FROM AUTHOR]

Breast cancer is a highly harmful malignant tumor, which poses a great threat to women's body and mind, and the mortality rate ranks second among all women's diseases. The incidence rate accounts for 7-10% of various malignant tumors in the whole body, second only to uterine cancer in women, and has become the main cause of threatening women's health. Advanced breast cancer is often considered an incurable disease. The family of heterogeneous nuclear ribonucleoprotein complexes is composed of about 20 hnRNP proteins with molecular weights ranging from 32 to 120 kDa, and they are named according to their molecular weights. Among them, hnRNPA2 and hnRNPB1 are the two most important members of the hnRNP family, both derived from the same gene on chromosome 7p15. Therefore, research to understand the molecular mechanism and process of breast cancer progression has an important role in promoting the current medical research on breast cancer treatment methods. Therefore, studying the mechanism of tumorigenesis is the key to tumor prevention and treatment. Therefore, this paper proposes that A2/B1 promotes the stability of NRF2 mRNA and inhibits ferroptosis and cell proliferation in breast cancer cells. The article mainly introduces the disease diagnosis method based on artificial neural network and its neural network algorithm. In the experimental part, the activity of hnRNP A2/B1 on cancer cells is deeply studied. The results show that the absorbance of the MTT method increases continuously with the extension of the culture time, and the maximum reaches 1.2. This fully shows that its absorption capacity is very strong, especially after 24 hours, the absorption rate rises from 0.6 to 0.9, which shows that 24 hours is the best absorption time. And it can also be found that hnRNPA2/B1 has a significant inhibitory effect on breast cancer cells; it can reduce the effect on breast cancer cell cycle and apoptosis. [ABSTRACT FROM AUTHOR]

The majority of Parkinson's disease (PD) is sporadic in elderly and is characterized by α-synuclein (αS) aggregation and other alterations involving mitochondria, ubiquitin-proteasome, and autophagy. The remaining are familial PD associated with gene mutations of either autosomal dominant or recessive inheritances. However, the former ones are similar to sporadic PD, and the latter ones are accompanied by impaired mitophagy during the reproductive stage. Since no radical therapies are available for PD, the objective of this paper is to discuss a mechanistic role for amyloidogenic evolvability, a putative physiological function of αS, among PD subtypes, and the potential relevance to therapy. Presumably, αS evolvability might benefit familial PD due to autosomal dominant genes and also sporadic PD during reproduction, which may manifest as neurodegenerative diseases through antagonistic pleiotropy mechanism in aging. Indeed, there are some reports describing that αS prevents apoptosis and mitochondrial alteration under the oxidative stress conditions, notwithstanding myriads of papers on the neuropathology of αS. Importantly, β-synuclein (βS), the nonamyloidogenic homologue of αS, might buffer against evolvability of αS protofibrils associated with neurotoxicity. Finally, it is intriguing to predict that increased αS evolvability through suppression of βS expression might protect against autosomal recessive PD. Collectively, further studies are warranted to better understand αS evolvability in PD pathogenesis, leading to rational therapy development. [ABSTRACT FROM AUTHOR]

Vision loss is primarily caused by age-related macular degeneration (AMD) due to oxidative retinal pigment epithelial (RPE) cell injury. Carotenoid utilization is deemed a possible strategy for treating AMD. Cordyceps militaris has advantages like immunomodulatory, anti-inflammatory, and antioxidative characteristics. This paper assessed the possible protective influence of carotenoids obtained by isolating and purifying the Cordyceps militaris (CMCT) into human RPE cells (ARPE-19) damaged by hydrogen peroxide (H2O2). The findings demonstrated that CMCT safeguarded the ARPE-19 cells against the damage and apoptosis caused by H2O2 and oxidative stress via Bcl-2 protein upregulation, as well as the expression of Bax and cleaved caspase-3 protein. In addition, CMCT treatment increased cell survival and restricted the generation of H2O2-induced reactive oxygen species (ROS) and the protein expression of NADPH oxidase-1 (NOX1). Additionally, the CMCT treatment of H2O2-induced ARPE-19 cells ameliorated high malondialdehyde (MDA) levels in oxidative stress-induced cells. The catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH) returned to standard levels, which were governed by the higher expression of nuclear Nrf2 protein in the ARPE-19 cells. Moreover, this study showed that CMCT safeguarded the ARPE-19 cells against the damage caused by oxidative stress via its antioxidant activity and antiapoptotic functionality, suggesting the potential therapeutic role of CMCT in AMD prevention and mitigation. [ABSTRACT FROM AUTHOR]

Objectıve. Ankaferd hemostat (ABS; Ankaferd Blood Stopper®) contains standardized plant extracts comprising Alpinia officinarum, Glycyrrhiza glabra, Thymus vulgaris, Urtica dioica, and Vitis vinifera. ABS especially was recognized for its hemostatic effect; however, antineoplastic role of ABS was identified during the last decade. The aim of this paper is to review the molecular basis and associated clinical implications of the ABS as a topical antineoplastic agent. Materials and Methods. Up to June 2022, literature searches were performed using the internet search engines Medline, Google Scholar, and Embase: Ankaferd. PRISMA flow diagram described the Ankaferd search. Results. ABS have important effects in several cellular processes, like control of the cell cycle, apoptosis, angiogenesis, signal transduction, inflammation, immunologic, and metabolic mechanisms. The molecular basis of antineoplastic roles of ABS depends on its proteomics, metabolomics, and transcriptomics features. ABS has antineoplastic effects on solid tumors like colon, bladder, breast, and osteosarcoma cancer cells. Also, ABS effects renal tubular apoptosis and has antitumoral roles on malign melanoma cells. ABS inhibits hematological tumors like myeloma and lymphoid cells. ABS induces apoptosis in retinal cells and has inhibitory effects on mesenchymal stem cells. It has an antiproliferative role on gastrointestinal tumors like hepatocellular carcinoma cells. Moreover, ABS has a treatment supportive role in cancer since it can prevent oxidative DNA damage and decrease the intestinal damage in necrotizing enterocolitis. Furthermore, it has chemopreventive and hepatoprotective features and can be used for prophylaxis and treatment of oral mucositis. Conclusion. ABS alters cell metabolism and cell cycle. ABS has antineoplastic role on cancer cells. The expanding context of ABS compromises anti-infective, antineoplastic, and wound healing features. ABS may also be used for the palliative, adjuvant, neoadjuvant, or supportive use by interventional radiology procedures for the treatment of solid tumors. Future controlled studies are necessary to clarify the pleiotropic role of ABS like antineoplastic, antithrombotic, anti-inflammatory, anti-infective, antifungal, and antioxidative effects. [ABSTRACT FROM AUTHOR]

Cholangiocarcinoma (CCA) is a hepatobiliary carcinoma characterized by the differentiation of bile duct cells, and the patients with CCA often have a poor prognosis. Eukaryotic translation initiation factor 5A (eIF5A) is reported to have multiple biological activities. Targeted activation of ferroptosis may be a therapeutic strategy for cancer. Nevertheless, the effects of eIF5A and ferroptosis on CCA are still elucidated. Our study explored the effects of eIF5A in CCA, and the mechanisms also are studied. In this paper, TCGA database analysis suggested that eIF5A was upregulated in CCA, and high expression of eIF5A might predict a poor prognosis. Moreover, FANCD2, SLC7A11, and HSPB1 were significantly overexpressed in CCA. The results indicated that eIF5A was overexpressed in CCA tissues and cells. Further experiments demonstrated that eIF5A silencing decreased CCA cell activity and enhanced ferroptosis and mitochondrial apoptosis. In addition, upregulation of eIF5A showed the opposite effect on CCA cells compared with downregulation of eIF5A. Finally, the silencing of eIF5A could restrain the growth of xenografted tumors and promote ferroptosis. Overall, eIF5A enlarged CCA cell activity and attenuated ferroptosis and mitochondrial apoptosis. The results suggested that assessment of eIF5A might provide help for the diagnosis and treatment of CCA. [ABSTRACT FROM AUTHOR]

A large number of facts have shown that epigenetic modification and metabolic reprogramming represented by noncoding RNA play an important role in the invasion and metastasis of breast cancer, but the mechanism is not clear. The purpose of our study is to find a new biomarker of breast cancer and to provide a new perspective for regulating glucose metabolism and aerobic glycolysis of BC. In this paper, by downregulating C-myc protein, our team found that the expression of long-chain noncoding RNATSPAR-AS2 was significantly downregulated. However, the expression of long-chain noncoding RNASPAR-AS2 in BC is relatively high, and the prognosis is poor. TSPEAR-AS2 can promote the malignant phenotype of BC cells, including proliferation, apoptosis, invasion and metastasis, and glycolysis. At the same time, TSPEAR-AS2 can also upregulate the expression of GLUT1, an important regulator of glycolysis, thus promoting the metabolic reprogramming of BC. Molecular mechanism experiments show that TSPEAR-AS2 may promote the expression of GLUT1 by participating in IGF2BP2 modified by the GLUT1 gene. Our results suggest that the C-myc/TSPEAR-AS2/GLUT1 axis promotes the invasion and metastasis of BC by inducing glucose metabolism reprogramming. However, more phenotypic and molecular mechanism results need to be further verified. [ABSTRACT FROM AUTHOR]

Background. Pyroptosis is a form of programmed cell death, playing a significant role in cancer. Glioblastoma multiforme (GBM) is the most common malignant brain tumor. The poor prognosis in GBM due to temozolomide (TMZ) resistance has been widely discussed. Such being the case, the correlation between TMZ resistance and pyroptosis is seldom investigated. On this basis, this paper aims to explore the potential prognostic value of genes related to TMZ resistance and pyroptosis as well as their relationship to the immune microenvironment in GBM. Methods. A total of 103 patients from TCGA were assigned to a training cohort; 190 from CGGA were assigned to a validation cohort. The prognostic risk model reflecting pyroptosis and TMZ resistance was built from the training cohort using multivariate Cox regression and performed validation. RT-qPCR was used to examine the expression of 4 genes from the risk signature. FOXP3 was selected for overexpression and verified using the western blot. The TMZ IC50 of FOXP3-overexpressed cell lines was determined by CCK8. Results. A four genes-based risk signature was established and validated, separating GBM patients into high- and low-risk groups. Compared with the low-risk group, the high-risk group presented worse clinical survival outcomes. Its differential expressed genes were enriched in immune-related pathways and closely related to the immune microenvironment. Moreover, RT-qPCR results suggested that FOXP3, IRF3, and CD274 were significantly upregulated in TMZ-resistant strains, while TP63 was downregulated. FOXP3-overexpressed GBM cell lines had higher TMZ IC50, implying an increased resistance of TMZ. Conclusion. A novel gene signature relevant to pyroptosis and TMZ resistance was constructed and could be used for the prognosis of GBM. The four genes from the risk model might play a potential role in antitumor immunity and serve as therapeutic targets for GBM. [ABSTRACT FROM AUTHOR]

Background. Osteoarthritis (OA) is a clinical joint degenerative disease, the pathogenic factors of which include age, obesity, and mechanical injury. Its main pathological features include cartilage loss, narrowing of joint space, and osteophyte formation. At present, there are a variety of treatment methods for OA. Natural products, which are gradually being applied in the treatment of OA, are advantageous as they present with low toxicity and low costs and act on multiple targets. Methods. The terms "natural products," "osteoarthritis," and "chondrocytes" were searched in PubMed to screen the related literature in the recent 10 years. Results. We comprehensively introduced 62 published papers on 48 natural products involving 6, 3, 5, 12, 4, and 5 kinds of terpenoids, polysaccharides, polyphenols, flavonoids, alkaloids, and saponins, respectively (and others). Conclusion. The mechanisms of their anti-OA action mainly involve reducing the production of inflammatory factors, reducing oxidative stress, regulating the metabolism of chondrocytes, promoting the proliferation of chondrocytes, or inhibiting chondrocyte apoptosis. This article summarizes the anti-OA activity of natural products in the last 10 years and provides candidate monomers for further study for use in OA treatment. [ABSTRACT FROM AUTHOR]

Isodon lophanthoides var. gerardianus (Benth.) H. Hara, a native medicinal plant produced chiefly across Southern China, is one of the mainstream varieties of Xihuangcao, which has long been applied in preventing and treating some common liver or gall diseases. Water-soluble total flavonoids (WSTF) extracted from folk herbal medicine have many pharmacological effects. The objective of the paper is to investigate the synergy of WSTF with 5-fluorouracil (5-FU) on HCC and the related mechanisms. Cells were exposed to WSTF alone or combination treatment with 5-FU. Then, in this study, we conducted cell viability test, cell cycle and clone forming test, apoptosis assay, reactive oxygen species (ROS), Western blotting, immunohistochemistry, and a xenograft tumor growth model for investigating the role of WSTF in HCC in vivo and in vitro. It was discovered that WSTF caused cell cycle arrest at the G0/G1 phase while increasing the ROS contents. The generation of ROS levels could cause cell apoptosis and inhibit colony formation. WSTF decreased the Bcl-2 level but promoted the Bax level. These showed the mitochondrial dependence of WSTF-mediated apoptosis. WSTF combined with 5-FU have a synergistic effect to significantly inhibit carcinogenicity in vivo and in vitro. The reduced ROS changed the synergy of WSTF with 5-FU. At last, WSTF inhibit the growth of HCC and promote the HCC sensitivity to 5-FU through ROS accumulation. WSTF-increased ROS levels may partially or completely contribute to enhanced toxicity. WSTF combined with 5-FU in HCC can play a synergistic effect when applied in the clinical setting. [ABSTRACT FROM AUTHOR]