Traditional Chinese Medicine Monomer Research Articles

Formulations of traditional Chinese medicine for the prevention and treatment of radiation-induced injury

The likelihood of radiation-induced injury (RII) has increased. Currently, the chemical drugs used to prevent and control radiation damage have some drawbacks, such as high toxicity, which can also have other side effects on the body. However, many traditional Chinese medicine (TCM) monomers, single TCM, and compound TCM preparations have shown good therapeutic effects against radiation damage with increased safety and minimal adverse reactions. Therefore, new anti-RII TCMs must be explored and developed. This study reviewed the TCM preparations for the prevention and treatment of RII and their mechanisms of action to provide a better theoretical basis for research on the prevention and treatment of RII. TCM is an efficient, safe, and convenient strategy for the prevention and treatment of RII. Graphical abstract: http://links.lww.com/AHM/A127.

Exploring the mechanisms of Qingdu Fang for the treatment of cervical HR-HPV using UPLC-QTOF-MS, network pharmacology, and cell experimentation.

Background: Qingdu Fang (QDF) is a traditional Chinese herbal formula with remarkable clinical effect in the treatment of HR-HPV, but its mechanism remains unclear. In this study, UPLC-QTOF-MS was used to detect its components, network pharmacology was used to explore the traditional Chinese medicine monomers and their related targets for the treatment of HR-HPV in QDF. Molecular docking and in vitro experiments were performed to verify the results. Methods: QDF constituents and active compounds were identified using UPLC-QTOF-MS analysis. TCMSP and GeneCard databases were used to identify active components, targets, and potential therapeutic targets in HR-HPV. PPI network was constructed using the String database to analyze protein-protein interactions. Cytoscape3.7.2 was used to construct PPI networks, while GO enrichment and KEGG pathway analyses with R. The effect of QDF on H8 cell proliferation was measured using the CCK-8 method, and apoptosis and cell cycle was assessed with flow cytometry. The effects of QDF on PI3K/AKT pathway were detected by Western blotting. Results: A total of 27 compounds were identified on QDF by UPLC-QTOF-MS. Base on Network pharmacology,a total of 254 target genes are involved in the action of QDF on cervical HR-HPV. PPI analysis suggested that TP53, JUN, AKT1, STAT3, TNF and IL6 were potential targets for QDF treatment of HR-HPV. Molecular docking shows that two compounds have strong binding activity with AKT1. CCK-8 and morphological observation have shown that QDF inhibits H8 cell proliferation in a dose-dependent manner. Flow cytometry experiments suggest that QDF induces apoptosis and cell cycle arrest in H8 cells. Western blotting experiments reveal that QDF inhibits the PI3K/AKT signaling pathway. Conclusion: QDF has a multi-faceted therapeutic approach for HR-HPV, targeting inflammation, oxidation, and apoptosis. It induces apoptosis in H8 cells by inhibiting the PI3K/AKT pathway.

Research progress of traditional Chinese medicine in regulating autophagy for intervening in diabetic cardiomyopathy

Diabetic cardiomyopathy(DCM) is a chronic complication of diabetes mellitus that leads to cardiac damage in the later stages of the disease, and its pathogenesis is complex, involving metabolic disorders brought about by a variety of aberrant alterations such as endoplasmic reticulum stress, oxidative stress, inflammation, and apoptosis, defects in cardiomyocyte Ca~(2+) transporter, and myocardial fibrosis. Currently, there is a lack of specific diagnosis and treatment in the clinic. Autophagy is a highly conserved scavenging mechanism that removes proteins, damaged organelles or foreign contaminants and converts them into energy and amino acids to maintain the stability of the intracellular environment. Inhibition of autophagy can cause harmful metabolites to accumulate in the cell, while over-activation of autophagy can disrupt normal cellular structures and cause cell death. Prolonged high glucose levels disrupt cardiomyocyte autophagy levels and exacerbate the development of DCM. The protective or detrimental effects of autophagy on cells ring true with the traditional Chinese medicine theory of healthy Qi and pathogenic Qi. Autophagy in the physiological state of the removal of intracellular substances and the generation of substances beneficial to the survival of cells is the inhibition of pathogenic Qi to help the performance of healthy Qi, so the organism is healthy. In the early stages of the disease, when autophagy is impaired and incapable of removing waste substances, pathogenic Qi is prevalent; In the later stages of the disease, excessive activation of autophagy can destroy normal cells, leading to a weakening of healthy Qi. Traditional Chinese medicine has the advantage of targeting multiple sites and pathways. Studies in recent years have confirmed that traditional Chinese medicine monomers or formulas can target autophagy, promote the restoration of autophagy levels, maintain mitochondrial and endoplasmic reticulum homeostasis, and reduce oxidative stress, endoplasmic reticulum stress, inflammation, and apoptosis in order to prevent and control DCM. This study provides a review of the relationship between autophagy and DCM and the intervention of traditional Chinese medicine in autophagy for the treatment of DCM, with a view to providing new clinical ideas and methods for the treatment of DCM with traditional Chinese medicine.

Integrating Network Pharmacology with in vitro Experiments to Validate the Efficacy of Celastrol Against Hepatocellular Carcinoma Through Ferroptosis.

As a traditional Chinese medicine monomer derived from Tripterygium wilfordii Hook.f. with potential anticancer activity, celastrol can induce ferroptosis in hepatic stellate cells and inhibit their activation to alleviate liver fibrosis. Activation of ferroptosis can effectively inhibit Hepatocellular carcinoma (HCC). Whether celastrol inhibits HCC by inducing ferroptosis remains to be studied. To explore the potential targets of celastrol against HCC through ferroptosis based on network pharmacology and to verify the anticancer effect of celastrol on HepG2 cells. We collected celastrol targets, HCC, and ferroptosis-related genes through online databases, and got their intersection targets. Subsequently, we obtained a protein-protein interaction (PPI) network, and performed gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to gain key genes for further study. They were verified in vitro and were performed molecular docking. The changes in cell proliferation and ferroptosis characteristics of HepG2 cells after celastrol treatment were detected. 31 core target genes were screened for PPI network and enrichment analysis. The most significantly related KEGG pathway was chemical carcinogenesis-reactive oxygen species. The mRNA and protein levels of GSTM1 were significantly decreased after celastrol treatment. Molecular docking demonstrated the interaction between celastrol and GSTM1. Ferroptosis was induced and cell proliferation was inhibited by celastrol in HCC cells. Celastrol induces ferroptosis in HCC via regulating GSTM1 expression and may serve as a novel therapeutic compound with clinical potential in HCC treatment.

Research Progress on Prevention and Treatment of Diabetes with Traditional Chinese Medicine Based on Intestinal Flora

In recent years, the World Health Organization has proposed the concept that only intestinal health can lead to longevity. It can be seen that gut microbiota plays an important role in maintaining human health, and gut microbiota has become a hot topic in medical research. With the change of Chinese residents' lifestyle, the incidence rate of diabetes is increasing rapidly. Research shows that the incidence of diabetes is closely related to intestinal flora imbalance. Traditional Chinese medicine can reduce blood sugar and improve clinical symptoms by regulating intestinal flora. Based on the theory of traditional Chinese medicine, this paper discusses the etiology and pathogenesis of intestinal flora imbalance, and provides a theoretical basis for traditional Chinese medicine to regulate intestinal flora to prevent and treat diabetes. Intestinal flora is a complex ecosystem, which plays an important role in maintaining human health. The imbalance of intestinal flora may lead to the occurrence of diabetes. The dynamic balance of gut microbiota is closely related to the kidneys, spleen, liver, and lungs. Traditional Chinese medicine monomer and compound can prevent and cure diabetes by regulating intestinal flora.

Research progress of nano-delivery systems for the active ingredients from traditional Chinese medicine.

Traditional Chinese medicine (TCM) has been used for thousands of years in China, characterizing with novel pharmacological mechanisms, low toxicity, and limited side effects. However, the application of TCM active ingredients is often hindered by their physical and chemical properties, including poor solubility, low bioavailability, short half-life, toxic side effects within therapeutic doses, and instability in biological environments. Consequently, an increasing number of researchers are directing their attention towards the discovery of nano-delivery systems for TCM to overcome these clinical challenges. This review aims to provide the latest knowledge and results concerning the studies on the nano-delivery systems for the active ingredients from TCM. Recent literature relating to nano-delivery systems for the active ingredients from TCM is summarized to provide a fundamental understanding of how such systems can enhance the application of phytochemicals. The nano-delivery systems of six types of TCM monomers are summarized and categorized based on the skeletal structure of the natural compounds. These categories include terpenoids, flavonoids, alkaloids, quinones, polyphenols, and polysaccharides. The paper analyzes the characteristics, types, materials used, and the efficacy achieved by TCM-nano systems. Additionally, the advantages and disadvantages of nano-drug delivery systems for TCM are summarized in this paper. Nano-delivery systems represent a promising approach to overcoming clinical obstacles stemming from the physical and chemical properties of TCM active ingredients, thereby enhancing their clinical efficacy.

Analysis of Clinical Trials Using Anti-Tumor Traditional Chinese Medicine Monomers

Analysis of Clinical Trials Using Anti-Tumor Traditional Chinese Medicine Monomers

Baicalein alleviates cisplatin-induced acute kidney injury by inhibiting ALOX12-dependent ferroptosis

BackgroundIn acute kidney injury (AKI), ferroptosis is the main mechanism of cell death in the renal tubular epithelium. Baicalein, a traditional Chinese medicine monomer, plays a protective role in various kidney diseases; however, the effect of baicalein on ferroptosis in AKI still needs further exploration. PurposeIn this study, we explored the role of baicalein and its specific mechanism in mediating ferroptosis in cisplatin-induced AKI. MethodsWe used a cisplatin-induced AKI model to study the effects of baicalein on renal tissue and tubular epithelial cell injury. The effects of baicalein on tubular epithelial cell ferroptosis were detected in cisplatin-induced AKI and further verified by folic acid-induced AKI. The Swiss Target Prediction online database was used to predict the possible mechanism by which baicalein regulates ferroptosis, and the specific target proteins were further verified. Molecular docking and SPR were used to further determine the binding potential of baicalein to the target protein. Finally, RNA interference (RNAi) technology and enzymatic inhibition were used to determine whether baicalein regulates ferroptosis through target proteins. ResultsBaicalein alleviated cisplatin- and folic acid-induced renal dysfunction and pathological damage and improved cisplatin-induced HK2 cell injury. Mechanistically, baicalein reduced the expression of 12-lipoxygenase (ALOX12), which inhibits phospholipid peroxidation and ferroptosis in AKI. Molecular docking and SPR demonstrated direct binding between baicalein and ALOX12. Finally, we found that silencing ALOX12 had a regulatory effect similar to that of baicalein. Comparable results were also obtained with the ALOX12 inhibitor ML355. ConclusionThis was the first study to confirm that baicalein regulates ferroptosis both in vitro and in vivo in cisplatin-induced AKI and to verify the regulatory effect of baicalein in folic acid-induced AKI. Our results reveal the critical role of ALOX12 in kidney damage and ferroptosis caused by cisplatin and emphasize the regulatory effect of baicalein on renal tubular epithelial cell ferroptosis mediated by ALOX12. Baicalein is an effective drug for treating AKI, and ALOX12 is a potential drug target.

Curculigoside, a traditional Chinese medicine monomer, ameliorates oxidative stress in Alzheimer's disease mouse model via suppressing ferroptosis.

Alzheimer's disease (AD) is a neurodegenerative disorder where oxidative stress, induced by ferroptosis, has been linked to neuronal damage and cognitive deficits. The objective of this study is to investigate if the potential therapeutic agent, Curculigoside (CUR), could ameliorate AD by inhibiting ferroptosis. The potential therapeutic targets, such as GPX4 and SLC7A11, were identified using weighted gene co-expression network analysis (WGCNA). Concurrently, CUR was also screened against these potential targets using various analytical methods. For the in vivo studies, intragastric administration of CUR significantly ameliorated cognitive impairment in AD model mice induced by scopolamine and okadaic acid (OA). In vitro, CUR protected neuronal cells by altering the levels of ferroptosis-related specific markers in OA and scopolamine-induced neurotoxicity. The administration of CUR through intragastric route significantly reduced the levels of AD-promoting factors (such as Aβ1-42, p-tau) and ferroptosis-promoting factors in the hippocampus and cortex of AD mice. Furthermore, CUR up-regulated the expression of GPX4 and decreased the expression of SLC7A11 in the ferroptosis signaling pathway, thereby increasing the ratio of glutathione (GSH)/oxidized glutathione (GSSG) in vivo and vitro. In conclusion, the cumulative results suggest that the natural compound CUR may serve as a promising therapeutic agent to ameliorate AD by inhibiting ferroptosis.

Astragaloside IV inhibits colorectal cancer metastasis by reducing extracellular vesicles release and suppressing M2-type TAMs activation

Ethnopharmacological relevanceTumour-derived extracellular vesicles (TEVs) have been confirmed to facilitate colorectal cancer (CRC) metastasis by remodelling the tumour microenvironment (TME). Drugs targeted TEVs is considered as a promising therapeutic strategy for cancer treatment. Traditional Chinese medicine (TCM) plays a vital role in improving the prognosis of CRC patients and eventually CRC patients with distant metastasis. Although the anti-tumour effects of active compounds from TCM prescriptions are observed widely, the molecular mechanisms remain unknown. Aim of the studyThis study aims to investigate the effects of active compounds in our library of TCM on preventing CRC metastasis, and also explore the potential mechanisms from the perspective of TEVs. Materials and methods: The effects of active compounds on the proliferation of CRC cells were determined by CCK-8 assay. TEVs were extracted from MC38 cells by ultracentrifugation and characterized by electron microscopy, Nanosight NS300 and western blotting. The TEV particles were quantified by Nanosight NS300. The potential mechanism by which astragaloside IV (ASIV) reduced TEV secretion was determined by western blotting. RAW264.7 cells were cocultured with the conditioned medium (CM) of MC38 cells treated with or without ASIV, and the activation of tumour-associated macrophages (TAMs) was assessed by immunofluorescence and quantitative polymerase chain reaction (qPCR). The migration of CRC cells was measured by wound healing and Transwell assay. A spleen-to-liver metastasis model of colorectal cancer was used to confirm the efficiency of ASIV in vivo. Liver metastatic tumours of the mice were used for liver weight measures and H&E staining. Immunofluorescence was applied to observe the infiltration of TAMs, the expression of neutral sphingomyelinase 2 (nSMase2) and Rab27a. ResultsBy screening our TCM monomer library, we found that ASIV, which is mainly extracted from Radix Astragali, reduced the release of TEVs from CRC cells in a time- and concentration-dependent manner. Mechanistically, ASIV inhibited the production and secretion of TEVs by downregulating nSMase2 and Rab27a expression in CRC cells. CM from ASIV-treated CRC cells reshaped the polarization of TAMs by decreasing M2-type polarization, increasing M1-type polarization. Consequently, the repolarization of M2-type to M1-type macrophages led to reduced invasion and migration of CRC cells. Moreover, we confirmed that ASIV inhibited the liver metastasis of CRC, reduced M2-type macrophage infiltration and decreased the expression of nSMase2 and Rab27a in liver metastases. ConclusionsASIV inhibited CRC metastasis by reducing EVs release and suppressing M2-type TAMs activation. All these findings reveal a new insight into the mechanisms of ASIV in preventing CRC progression and provide a promising approach for anti-tumour therapy.

Research Progress of traditional Chinese Medicine monomers in Vascular Protection

Research Progress of traditional Chinese Medicine monomers in Vascular Protection

Loureirin A is a narrow-spectrum antimicrobial agent against Helicobacter pylori.

Currently, Helicobacter pylori eradication by antibiotic therapy faces various challenges, including antibiotic resistance, side effects on intestinal commensal bacteria, and patient compliance. In this study, loureirin A (LrA), a traditional Chinese medicine monomer extracted from Sanguis Draconis flavones, was found to possess specific antibacterial activity against H. pylori without the bacteria displaying a tendency to develop resistance in vitro. LrA demonstrated a synergistic or additive effect when combined with omeprazole (a proton pump inhibitor) against H. pylori. The combination of LrA and omeprazole showed promising anti-H. pylori potential, exhibiting notable in vivo efficacy comparable to standard triple therapy in mouse models infected with both drug-sensitive and drug-resistant H. pylori strains. Moreover, the narrow-spectrum antibacterial profile of LrA is reflected in its minimal effect on the diversity and composition of the mouse gut microbiota. The underlying mechanism of action of LrA against H. pylori involves the generation of bactericidal levels of reactive oxygen species, resulting in apoptosis-like cell death. These findings indicate that LrA is a promising lead compound targeting H. pylori without harming the commensal bacteria.

Preparation of mesoporous silica/hydroxyapatite loaded quercetin nanoparticles and research on its antibacterial properties

In this study, amino-functionalized mesoporous silica/hydroxyapatite nanoparticles (MSNS/HAP) with the property of acid dissociation have been prepared as a traditional Chinese medicine monomer carriers to improve the drug loading rate and antibacterial properties of antimicrobial quercetin (QUE) in vitro. The experimental results confirm that the drug loading rate of MSNs/HAP is 28.94 %, which is about 3.6 times higher than that of aminated mesoporous sililca nanoparticles (MSNs). The drug release of QUE on MSNs/HAP is pH-sensitive in phosphate buffered saline (pH=4.0–7.4). The above fabricated traditional Chinese medicine monomer modified nanocomposites (QUE@MSNs/HAP) displays concentration-dependent inhibitory effect, which shows better antibacterial effect than free QUE. The minimum inhibitory concentration for two tested bacteria, Staphylococcus aureus (S.aureus) and Escherichia coli (E.coli), is 256 mg·L −1. In summary, QUE@MSNs/HAP have successfully prepared, which not only improves the bio-availability of QUE, but also has acid-sensitive drug release properties. Compared with free QUE, its antibacterial performance significantly enhances, which provides a theoretical basis for the application of Chinese medicine molecules in bacterial treatment.

The Application and Pathway Regulation of Traditional Chinese Medicine in Lung Cancer Treatment: An Exploratory Review

Lung cancer is one of the cancers with the highest mortality rate. Non-small cell lung cancer (NSCLC) accounts for 85% of lung cancer cases and is often diagnosed at an advanced stage with a poor prognosis. Due to the lack of effective molecular targets, the current clinical cure rate is low, and the recurrence rate is high. Recent studies have found that active components of traditional Chinese medicine and Chinese herbal formulas can inhibit the development of NSCLC through multiple pathways and targets, effectively reducing its metastasis and recurrence rates, improving treatment side effects, and compensating for the deficiencies in drug resistance. Although treatments such as surgery, radiotherapy, targeted therapy, and immunotherapy have achieved better clinical efficacy in treating lung cancer, they still have problems such as multiple complications and severe adverse reactions. In recent years, numerous basic and clinical studies have confirmed the good effects of traditional Chinese medicine in treating lung cancer. Traditional Chinese medicine has a synergistic regulatory effect through multiple components, targets, pathways, and channels. The numerous active monomeric components and complex mechanisms of action determine that there are issues such as unclear related mechanisms of action in the prevention and treatment of lung cancer by traditional Chinese medicine. There is an urgent need to elucidate the mechanisms of action of traditional Chinese medicine in intervening lung cancer from the perspective of modern medicine, and at the levels of molecular biology, network pharmacology, etc. This article systematically summarizes the research progress on the regulation of the above-mentioned signaling pathways and the expression of key protein molecules by traditional Chinese medicine monomers or formulas, aiming to clarify the mechanisms of action of traditional Chinese medicine in the progression of lung cancer, and to provide ideas and theoretical basis for the in-depth study and clinical application of traditional Chinese medicine in intervening lung cancer.

Traditional Chinese medicine bufalin inhibits infectious hematopoietic necrosis virus infection in vitro and in vivo.

Infectious hematopoietic necrosis virus (IHNV) is the pathogen of infectious hematopoietic necrosis (IHN) which outbreak often causes huge economic losses and hampers the healthy development of salmon and trout farming. Currently, there is only one approved DNA vaccine for IHN worldwide, but it faces some biosafety problems. Hence, more effective vaccines and antiviral drugs are needed to prevent IHNV infection. In this study, we report that bufalin, a traditional Chinese medicine, shows potential antiviral activity against IHNV both in vitro and in vivo. The bufalin-mediated block of IHNV infection occurred at the viral attachment and RNA replication stages, but not internalization, and bufalin inhibited IHNV infection by targeting Na+/K+-ATPase. The in vitro and in vivo studies showed that bufalin significantly inhibited IHNV infection and may be a promising candidate drug against the disease in rainbow trout.

Treatment of Intracerebral Hemorrhage with Traditional Chinese Medicine Monomer Wogonin by Modifying NLRP3 with METTL14 to Inhibit Neuronal Cell Pyroptosis.

The aim of this study was to investigate the alleviating effect of wogonin on intracerebral hemorrhage (ICH) and its mechanism. The hemin-treated PC-12 cells were constructed to mimic ICH in vitro. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) analysis was used for cell viability measurement and flow cytometry was for pyroptosis detection. Enzyme-linked immunosorbent assay (ELISA) assay and western blot were used to detect the protein levels of pyroptosis-related proteins. The modification level of N6-methyladenosine (m6A) methylation was detected by quantitative real-time polymerase chain reaction (qRT-PCR) combined with m6A dot blot assays. Molecular docking experiments analyzed the binding of wogonin and METTL14 protein. The correlation between METTL14 and NLRP3 was confirmed by bioinformatics analysis and dual luciferase reporter gene detection. ICH was induced in mice injected with collagenase into the basal ganglia, and the neurobehavioral damage was evaluated. Triphenyltetrazolium chloride monohydrate (TTC) staining and neurological scores were used to assess brain damage in mice. The results demonstrated that wogonin alleviated neuronal cell pyroptosis, and was molecularly docked with METTL14. Overexpression of METTL14 partly reversed the protecting effects of wogonin on brain in vitro and in vivo. Furthermore, NLRP3 was methylated by METTL14. Taken together, wogonin inhibits neuronal pyroptosis and thus treats IHC by inhibiting METTL14 and its methylated NLRP3.

Drug screening identified that handelin inhibits feline calicivirus infection by inhibiting HSP70 expression in vitro.

Feline calicivirus (FCV) is considered one of the major pathogens of cats worldwide and causes upper respiratory tract disease in all cats. In some cats, infection is by a highly virulent strain of FCV (vs.-FCV), which can cause severe and fatal systemic disease symptoms. At present, few antiviral drugs are approved for clinical treatment against FCV. Therefore, there is an imminent need for effective FCV antiviral agents. Here, we used observed a cytopathic effect (CPE) assay to screen 1746 traditional Chinese medicine monomer compounds and found one that can effectively inhibit FCV replication, namely, handelin, with an effective concentration (EC50) value of approximately 2.5 µM. Further study showed that handelin inhibits FCV replication via interference with heat shock protein 70 (HSP70), which is a crucial host factor and plays a positive role in regulating viral replication. Moreover, handelin and HSP70 inhibitors have broad-spectrum antiviral activity. These findings indicate that handelin is a potential candidate for the treatment of FCV infection and that HSP70 may be an important drug target.

Coumestrol facilitates apoptosis in colorectal cancer cells by interacting with ZIP8 protein via the ferroptosis pathway.

Objective: So far, there have been no reports of coumestrol inhibiting colorectal cancer (CRC) through the ferroptosis pathway. This study is to investigate the mechanism of the traditional Chinese medicine monomer coumestrol in the treatment of CRC. Methods: Data on CRC transcriptome sequencing was obtained from the GEO database and TCGA database. Bioinformatics analyses were conducted to screen for CRC prognostic-related key genes and their potential binding monomers in traditional Chinese medicine. The inhibitory effect of coumestrol on CRC cell lines (COLO 205 & HCT 116) was determined using the CCK-8 assay, and cell apoptosis was assessed by flow cytometry. The content of ferrous ions was measured using the Ferrous Ion Content Assay Kit. The expression of ferroptosis pathway-related genes SLC39A8, NCOA4, VDAC2, and NOX2 before and after small interference RNA (siRNA) was examined through real-time PCR and Western blotting. Results: SLC39A8 was found to be associated with CRC clinical progression staging, and its encoded protein ZIP8 may bind to coumestrol. KEGG enrichment analysis suggested that ZIP8 plays a role in iron transmembrane transport and may affect the expression of ferroptosis pathway-related genes NCOA4, VDAC2, and NOX2. Coumestrol was found to induce apoptosis in CRC cell lines by upregulating the expression of ferroptosis pathway-related genes SLC39A8, NCOA4, VDAC2, and NOX2. However, coumestrol was unable to upregulate the expression of ferroptosis pathway-related genes in CRC cell lines after SLC39A8 interference. Conclusion: Coumestrol facilitates apoptosis in CRC cells by interacting with ZIP8 protein via the ferroptosis pathway.

Harnessing the power of traditional Chinese medicine monomers and compound prescriptions to boost cancer immunotherapy.

At present, cancer is the largest culprit that endangers human health. The current treatment options for cancer mainly include surgical resection, adjuvant radiotherapy and chemotherapy, but their therapeutic effects and long-term prognosis are unsatisfactory. Immunotherapy is an emerging therapy that has completely transformed the therapeutic landscape of advanced cancers, and has tried to occupy a place in the neoadjuvant therapy of resectable tumors. However, not all patients respond to immunotherapy due to the immunological and molecular features of the tumors. Traditional Chinese Medicine (TCM) provides a new perspective for cancer treatment and is considered to have the potential as promising anti-tumor drugs considering its immunoregulatory properties. This review concludes commonly used TCM monomers and compounds from the perspective of immune regulatory pathways, aiming to clearly introduce the basic mechanisms of TCM in boosting cancer immunotherapy and mechanisms of several common TCM. In addition, we also summarized closed and ongoing trials and presented prospects for future development. Due to the significant role of immunotherapy in the treatment of non-small cell lung cancer (NSCLC), TCM combined with immunotherapy should be emphasized in NSCLC.

Asiatic acid affects the growth of human osteosarcoma cells by regulating PI3K/AKT and NF-κB dual signal pathways

Osteosarcoma(OS) is a common primary malignant bone tumor, which mostly occurs in children and adolescents. Currently, chemotherapy drugs for the clinical treatment of OS have high side effects and patients are prone to chemotherapy resistance, which reduces the therapeutic effect. Therefore, the development of new therapeutic drugs is very important to reduce the toxicity and adverse reactions of drugs and improve the survival rate of patients. At present, the antitumor activity of traditional Chinese medicine monomers has received extensive attention because of its safety and efficacy. Asiatic acid (AA) is a naturally pentacyclic triterpenoids extracted from Centella asiatica. The aim of this study was to evaluate the effect and mechanism of AA on OS cells in vitro and in vivo. In vitro results showed that AA inhibited the proliferation, migration and invasion of OS cells and was able to induce apoptosis and cycle arrest. In vivo results showed that AA inhibited the growth of OS and the size of lung metastasis in nude mice. Network pharmacology, molecular docking and in vitro experiments prove that AA may play a role in the treatment of OS by inhibiting PI3K/AKT and NF-κB signaling pathways. Our study shows that AA can act on multiple targets of OS and regulate multiple pathways to intervene in the occurrence and development of OS, which may provide reference for the clinical application and development of AA.