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Cancer, a chronic disease characterized by uncontrolled cell development, kills millions of people globally. The WHO reported over 10 million cancer deaths in 2020. Anticancer medications destroy healthy and malignant cells. Cancer treatment induces neuropathy. Anticancer drugs cause harm to spinal cord, brain, and peripheral nerve somatosensory neurons, causing chemotherapy-induced neuropathic pain. The chemotherapy-induced mechanisms underlying neuropathic pain are not fully understood. However, neuroinflammation has been identified as one of the various pathways associated with the onset of chemotherapy-induced neuropathic pain. The neuroinflammatory processes may exhibit varying characteristics based on the specific type of anticancer treatment delivered. Neuroinflammatory characteristics have been observed in the spinal cord, where microglia and astrocytes have a significant impact on the development of chemotherapy-induced peripheral neuropathy. The patient's quality of life might be affected by sensory deprivation, loss of consciousness, paralysis, and severe disability. High cancer rates and ineffective treatments are associated with this disease. Recently, histone deacetylases have become a novel treatment target for chemotherapy-induced neuropathic pain. Chemotherapy-induced neuropathic pain may be treated with histone deacetylase inhibitors. Histone deacetylase inhibitors may be a promising therapeutic treatment for chemotherapy-induced neuropathic pain. Common chemotherapeutic drugs, mechanisms, therapeutic treatments for neuropathic pain, and histone deacetylase and its inhibitors in chemotherapy-induced neuropathic pain are covered in this paper. We propose that histone deacetylase inhibitors may treat several aspects of chemotherapy-induced neuropathic pain, and identifying these inhibitors as potentially unique treatments is crucial to the development of various chemotherapeutic combination treatments.Graphical Abstract: Cancer, a chronic disease characterized by uncontrolled cell development, kills millions of people globally. The WHO reported over 10 million cancer deaths in 2020. Anticancer medications destroy healthy and malignant cells. Cancer treatment induces neuropathy. Anticancer drugs cause harm to spinal cord, brain, and peripheral nerve somatosensory neurons, causing chemotherapy-induced neuropathic pain. The chemotherapy-induced mechanisms underlying neuropathic pain are not fully understood. However, neuroinflammation has been identified as one of the various pathways associated with the onset of chemotherapy-induced neuropathic pain. The neuroinflammatory processes may exhibit varying characteristics based on the specific type of anticancer treatment delivered. Neuroinflammatory characteristics have been observed in the spinal cord, where microglia and astrocytes have a significant impact on the development of chemotherapy-induced peripheral neuropathy. The patient's quality of life might be affected by sensory deprivation, loss of consciousness, paralysis, and severe disability. High cancer rates and ineffective treatments are associated with this disease. Recently, histone deacetylases have become a novel treatment target for chemotherapy-induced neuropathic pain. Chemotherapy-induced neuropathic pain may be treated with histone deacetylase inhibitors. Histone deacetylase inhibitors may be a promising therapeutic treatment for chemotherapy-induced neuropathic pain. Common chemotherapeutic drugs, mechanisms, therapeutic treatments for neuropathic pain, and histone deacetylase and its inhibitors in chemotherapy-induced neuropathic pain are covered in this paper. We propose that histone deacetylase inhibitors may treat several aspects of chemotherapy-induced neuropathic pain, and identifying these inhibitors as potentially unique treatments is crucial to the development of various chemotherapeutic combination treatments. [ABSTRACT FROM AUTHOR]

Six new C 21 steroidal glycosides ( 1 – 6 ) and one dideoxysaccharide ( 7 ), named atratcynosides A–F and atratcynose A, were isolated from the 80% ethanol extract of the root of Cynanchum atratum , together with three known compounds ( 8 – 10 ). The structures of the new compounds were determined on the basis of extensive spectral analyses and qualitative chemical methods. All compounds were subjected to detect the immunosuppressive activities by an in vitro model of concanavalin A-induced proliferation of T-lymphocytes from mice. Compounds 1 – 3 showed significant immunosuppressive activities in dose-dependent manners with the IC 50 values from 3.3 to 7.0 μM. Moreover, the structure–activity relationship of the steroidal glycosides on the immunosuppression was analyzed. [ABSTRACT FROM AUTHOR]

The present study focuses on the biological synthesis, characterization, and antibacterial activities of silver nanoparticles (AgNPs) using extracellular extracts of Aspergillus japonicus PJ01.The optimal conditions of the synthesis process were: 10 mL of extracellular extracts, 1 mL of AgNO3 (0.8 mol/L), 4 mL of NaOH solution (1.5 mol/L), 30 °C, and a reaction time of 1 min. The characterizations of AgNPs were tested by UV-visible spectrophotometry, zeta potential, scanning electron microscope (SEM), transmission electron microscopy (TEM), X-ray diffraction (XRD), and thermogravimetric (TG) analyses. Fourier transform infrared spectroscopy (FTIR) analysis showed that Ag+ was reduced by the extracellular extracts, which consisted chiefly of soluble proteins and reducing sugars. In this work, AgNO3 concentration played an important role in the physicochemical properties and antibacterial properties of AgNPs. Under the AgNO3 concentration of 0.2 and 0.8 mol/L, the diameters of AgNPs were 3.8 ± 1.1 and 9.1 ± 2.9 nm, respectively. In addition, smaller-sized AgNPs showed higher antimicrobial properties, and the minimum inhibitory concentration (MIC) values against both E. coli and S. aureus were 0.32 mg/mL. [ABSTRACT FROM AUTHOR]