Pancreatic cancer progression is closely associated with metabolic remodeling, and a lipid-enriched microenvironment may further promote tumor cell growth and survival. Diosgenin has reported anti-tumor and lipid metabolism-regulatory activities, but its poor aqueous solubility limits its biological application. In this study, diosgenin-loaded DSPE-PEG liposomes (Dio@Lipo) were prepared as a sustained delivery system and evaluated in pancreatic cancer cells under high-fat conditions. Dio@Lipo showed nanoscale morphology, relatively narrow particle size distribution, negative zeta potential, sustained release behavior, and preliminary hemocompatibility. A high-fat in vitro model was established using a free fatty acid mixture of sodium oleate and sodium palmitate. Under this condition, SW1990 and PANC-1 cells showed increased viability and upregulated lipid metabolism-related proteins, supporting the establishment of a lipid-enriched cellular state. Dio@Lipo reduced high-fat-associated cell viability in both cell lines and altered cell-cycle distribution. Western blot analysis showed that Dio@Lipo treatment was accompanied by increased Bax and cleaved caspase-3 expression, decreased Bcl-2 expression, and reduced levels of FABP4, FASN, and PLIN2. Network pharmacology, molecular docking, and FABP4-related bioinformatics analyses were used as supplementary evidence to explore potential lipid metabolism-associated targets. Overall, this study supports Dio@Lipo as a simple liposomal sustained delivery system with preliminary in vitro inhibitory activity against high-fat-associated pancreatic cancer cell growth.

Inflammation and oxidative stress play crucial roles in the pathogenesis of diabetic kidney disease (DKD). Hirudin, a small molecular polypeptide derived from the salivary glands of leeches, is widely utilized in anti-coagulation and antithrombotic therapies. However, the effects and underlying molecular mechanisms of hirudin on DKD remain unclear. Db/db mice were employed to evaluate the effects of hirudin on DKD. Key parameters assessed included urinary albumin, oral glucose tolerance, glomerular diameter, and the expression levels of NLRP3, IL-1β, IL-18, caspase-1, and reactive oxygen species (ROS). Additionally, proteomic analysis was performed to measure the β-hydroxybutyrylation level of SOD2, and the effects of changes in SOD2 β-hydroxybutyrylation were evaluated by immunoprecipitation. In vivo experiments demonstrated that hirudin significantly improved urinary albumin levels, oral glucose tolerance, and glomerular diameter in diabetic mice. Furthermore, the β-hydroxybutyrylation level of SOD2 was reduced, leading to decreased production of ROS and suppression of NLRP3 inflammasome activation. In vitro experiments indicated that hirudin reduced the polarization of RAW264.7 cells, lowered their ROS levels, diminished NLRP3 inflammasome activation, and reduced the β-hydroxybutyrylation modification level of SOD2. Hirudin can alleviate the progression of DKD by reducing the β-hydroxybutyrylation level of SOD2, which in turn reduces ROS production and NLRP3 inflammasome activation, thereby suppressing inflammation. These findings provide new insights into the potential application of hirudin in the context of DKD.

Non-alcoholic steatohepatitis-associated hepatocellular carcinoma (NASH-HCC) accounts for an increasing proportion of HCC cases. Currently, effective pharmacological options for treating both NASH and NASH-HCC remain limited, necessitating the identification of novel therapeutic agents. Our previous studies have demonstrated that ginger can ameliorate nonalcoholic fatty liver disease (NAFLD) and prevent the occurrence of NASH. The therapeutic effects and underlying mechanisms of NASH-HCC, however, remain poorly understood. Network pharmacology, bioinformatics, single-cell RNA sequencing analysis, and molecular docking were used to identify the main active compounds, targets, and possible mechanisms of ginger in treating NASH-HCC. The anti-tumor efficacy and underlying mechanisms of the selected compound in treating NASH-HCC were validated through in vitro experimentation. Network pharmacology, bioinformatics, and molecular docking have revealed that 6-gingerol is the main active compound of ginger in treating NASH-HCC. SRC can be an essential target gene for ginger attenuating NASH-HCC progression, while the mitogen-activated protein kinase (MAPK) signaling pathway and reactive oxygen species (ROS) play equally important roles. Single-cell RNA sequencing of the HCC patients shows that the key targets of ginger in treating NASH-HCC are distributed in tumor-associated macrophage (TAMs). It has been reported that NOX2-derived ROS in macrophages can activate Src and then regulate downstream MAPK signaling cascades. 6-Gingerol can inhibit the proliferation, migration and reduce lipid deposition of liver cancer cells in vitro. More importantly, it induces polarization TAMs to M1 and enhances proinflammatory function, which may be achieved via the NOX2/Src/MAPK signaling pathway. This study proves that 6-gingerol, the primary active compound in ginger, plays a role in attenuating the progression of NASH-HCC by inhibiting the proliferation and migration of tumor cells, or reprogramming TAMs to the M1 phenotype via the NOX2/Src/MAPK signaling pathway and activating the TAM-mediated immune responses.

Tubular injury and oxidative stress are involved in the pathogenesis of diabetic kidney disease (DKD). Astragaloside IV (ASIV) is a natural antioxidant. The effects and underlying molecular mechanisms of ASIV on DKD have not been elucidated. The db/db mice and high-glucose-stimulated HK2 cells were used to evaluate the beneficial effects of ASIV in vivo and in vitro. Succinylated proteomics was used to identify novel mechanisms of ASIV against DKD and experimentally further validated. ASIV alleviated renal dysfunction and proteinuria, downregulated fasting blood glucose, and upregulated insulin sensitivity in db/db mice. Meanwhile, ASIV alleviated tubular injury, oxidative stress, and mitochondrial dysfunction in vivo and in vitro. Mechanistically, ASIV reversed downregulated 17beta-hydroxysteroid dehydrogenase type 10 (HSD17B10) lysine succinylation by restoring carnitine palmitoyl-transferase1alpha (Cpt1a or CPT1A) activity in vivo and in vitro. Molecular docking and cell thermal shift assay revealed that ASIV may bind to CPT1A. Molecular dynamics simulations demonstrated K99 succinylation of HSD17B10 maintained mitochondrial RNA ribonuclease P (RNase P) stability. The K99R mutation of HSD17B10 induced oxidative stress and disrupted its binding to CPT1A or mitochondrial ribonuclease P protein 1 (MRPP1). Importantly, ASIV restored the interaction between HSD17B10 and MRPP1 in vivo and in vitro. We also demonstrated that ASIV reversed high-glucose-induced impaired RNase P activity in HK2 cells, which was suppressed upon K99R mutation of HSD17B10. These findings suggest that ASIV ameliorates oxidative stress-associated proximal tubular injury by upregulating CPT1A-mediated K99 succinylation of HSD17B10 to maintain RNase P activity.

In this study, we aimed to investigate the protective effects of Panax notoginseng and leech (PL) on renal fibrosis and explore the mechanisms underlying their actions. For this study, we created an adenine-induced renal fibrosis model in SD rats to investigate the protective effect of PL on renal fibrosis and explore its underlying mechanism. Initially, we assessed the renal function in RF rats and found that Scr, BUN, and urine protein content decreased after PL treatment, indicating the protective effect of PL on renal function. Histological analysis using HE and Masson staining revealed that PL reduced inflammatory cell infiltration and decreased collagen fiber deposition in renal tissue. Subsequently, we analyzed the levels of α-SMA, Col-IV, and FN, which are the main components of the extracellular matrix (ECM), using IHC, RT-qPCR, and WB. The results demonstrated that PL was effective in reducing the accumulation of ECM, with PL1-2 showing the highest effectiveness. To further understand the underlying mechanisms, we conducted UPLC-MS/MS analysis on the incoming components of the PL1-2 group. The results revealed several associations between the differential components and antioxidant and mitochondrial functions. This was further confirmed by enzyme-linked immunosorbent assay and biochemical indexes, which showed that PL1-2 ameliorated oxidative stress by reducing ROS and MDA production and increasing GSH and SOD levels. Additionally, transmission electron microscopy results indicated that PL1-2 promoted partial recovery of mitochondrial morphology and cristae. Finally, using RT-qPCR and WB, an increase in the expression of mitochondrial fusion proteins Mfn1, Mfn2, and Opa1 after PL1-2 treatment was observed, coupled with a decline in the expression and phosphorylation of mitochondrial cleavage proteins Fis and Drp1. These findings collectively demonstrate that PL1-2 ameliorates renal fibrosis by reducing oxidative stress and restoring mitochondrial balance.

Chronic renal failure (CRF) causes a reduction in glomerular filtration rate and damage to renal parenchyma. Fushengong decoction (FSGD) showed improvement in renal function in CRF rats. This study aims to analyze the differentially expressed proteins in CRF patients treated with Western medicine alone or in combination with FSGD. Sixty patients with CRF recruited from Yongchuan Traditional Chinese Medicine Hospital affiliated to Chongqing Medical University were randomly assigned into control (treated with Western medicine alone) and observation groups (received additional FSGD treatment thrice daily for 8 weeks). The clinical efficacy and changes in serum Bun, serum creatinine, Cystatin C, and transforming growth factor beta 1 (TGF-β1) before and after treatment were observed. We employed isotope relative labeling absolute quantification labeling and liquid chromatography–mass spectrometry to identify differentially expressed proteins and carried out bioinformatics Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses. Patients in the observation group showed greater clinical improvement and lower levels of serum Bun, serum creatinine, Cyc-c, and TGF-β1 than the control group. We identified 32 differentially up-regulated and 52 down-regulated proteins in the observation group. These proteins are involved in the blood coagulation system, protein serine/threonine kinase activity, and TGF-β, which are closely related to the pathogenesis of CRF. Protein–protein-interaction network analysis indicated that candidate proteins fibronectin 1, fibrinogen alpha chain, vitronectin, and Serpin Family C Member 1 were in the key nodes. This study provided an experimental basis suggesting that FSGD combined with Western medicine could significantly improve renal function and renal fibrosis of CRF patients, which may be through the regulation of fibronectin 1, fibrinogen alpha chain, vitronectin, Serpin Family C Member 1, TGF-β, and the complement coagulation pathway (see Graphical abstract S1, Supplemental Digital Content, http://links.lww.com/MD/L947).

ETHNOPHARMACOLOGICAL RELEVANCE:Formononetin (FMN), one of the main isoflavones isolated from Astragalus membranaceus (Fisch.) Bunge, has multiple pharmacological and renal-protective effects. Our previous study suggested FMN as a candidate compound for the treatment of chronic renal failure (CRF). However, the mechanism underlying the repressive effect of FMN on the development of CRF is still unknown. AIMS OF THE STUDY:To investigate the protective effect of FMN on CRF using in vivo and in vitro models and elucidate the potential underlying mechanism. MATERIALS AND METHODS:An in vivo model of adenine-induced CRF and an in vitro model of human proximal tubule epithelial cells (HK-2) stimulated with transforming growth factor (TGF)-β1 were used. Serum levels of renal function parameters and inflammatory cytokines were evaluated. Histological analysis was performed to determine the extent of renal injury and fibrosis. Network pharmacology and mRNA sequencing were used to explore the potential mechanism. PPI analysis and molecular docking were used to identify key targets. Polymerase chain reaction and western blotting were used to determine the mechanism underlying the effect of FMN on CRF. RESULTS:FMN decreased the levels of renal function biochemical markers, including serum creatinine, blood urea nitrogen, and 24 h urine protein content. Treatment with FMN improved renal tubule injury and extracellular matrix (ECM) components, including collagens I and III. In addition, FMN significantly inhibited epithelial-mesenchymal transition (EMT); decreased the expression of fibronectin, N-cadherin, vimentin, α-SMA, and TGF-β1; and restored the expression of E-cadherin. The effect of FMN on renal interstitial fibrosis contributed to decreasing the expression of PI3K, p-Akt, and interleukin (IL) 4, restoring the expression of nitric oxide synthase 3 (NOS3), and reducing the release of inflammatory cytokines (IL-1β, IL-6, and tumor necrosis factor-alpha), both in vivo and in vitro. FMN treatment improved renal function and deposition of ECM components, reduced protein levels of EMT markers in rat kidneys and HK-2 cells, decreased the release of inflammatory cytokines, and inhibited the PI3K/Akt signaling pathway. CONCLUSIONS:FMN treatment significantly reduced the release of inflammatory cytokines and inhibited the effects of the PI3K/Akt signaling pathway on the key targets IL-4 and NOS3. Our results suggest FMN therapy as a novel therapeutic strategy for treating CRF.

慢性萎缩性胃炎(chronic atrophic gastritis,CAG)是以胃黏膜萎缩、固有腺体减少,常伴有不同程度的肠腺化生、幽门腺化生或不典型增生为特征的慢性胃部疾病[1],具有病程长、治疗难、易反复的特点.该病已被公认为胃癌前病变,一般按照"萎缩性胃炎→肠化生→异型增生→胃癌"的规律进展[2],胃黏膜萎缩程度与胃癌发生的风险呈显著正相关[3],如何延缓或逆转胃粘膜萎缩成为了预防胃癌发生的重要突破口.

老年类风湿关节炎(RA)包括年龄60岁以上发病的RA患者(EORA)以及中青年发病的RA患者(YORA)迁延至老年.随着全球的老龄化,RA患者及合并多种慢性病的患者日益增多,中国健康与养老截至2021年3月追踪调查(CHARLS)的统计数据显示,我国中老年人与其他慢性病共同发生概率最高的疾病为关节炎或风湿病,占总调查人群的58.23％[1].RA的临床表现、相关检查以及用药均有其特点.通过对涉及RA的相关研究结果进行整理与探讨,可进一步加深对该疾病的认识.

Polycystic ovary syndrome (PCOS) is characterized by reproductive, endocrine, and metabolic disorders. Icariin has been shown to regulate endocrine and metabolic imbalances. This study aimed to determine the therapeutic effect and pharmacological mechanism of icariin in PCOS rats. Rats were fed a high-fat diet and gavaged with letrozole to induce PCOS. Thirty-six female rats were randomly divided into four groups: control, model, low-dose, and high-dose icariin. After 30 days of treatment, we evaluated the therapeutic effects on weight and diet, sex hormone levels, ovarian morphology, estrous cycle, inflammatory factors, and indicators of glucolipid metabolism. Combined with the ovarian transcriptome, we verified the key markers of apoptosis and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway by RT-qPCR for mRNA level, western blot, and immunohistochemistry for protein expression. Icariin significantly improved ovarian function and reproductive endocrine disorders by regulating sex hormones, restoring the estrous cycle, and reducing ovarian morphological damage in PCOS rats. Icariin-treated rats had lower weight gain and reduced triglycerides, fasting insulin, HOMA-IR, TNF-α, and interleukin-6 with higher high-density lipoprotein cholesterol levels than PCOS rats. TUNEL staining showed icariin improved apoptosis in the ovaries. This was supported by an increase in Bcl2 and a decrease in Bad and Bax. Icariin decreased the ratios of p-JAK2/JAK2, p-STAT1/STAT1, p-STAT3/STAT3, and p-STAT5a/STAT5a, decreased IL-6, gp130 expression, and increased cytokine-inducible SH2-containing protein (CISH) and suppressor of cytokine signaling 1 (SOCS1) expression. The pharmacological mechanism may be related to the reduction in ovarian apoptosis and inhibition of the IL-6/gp130/JAK2/STATs pathway.

类风湿性关节炎(rheumatoidarthritis,RA)是以关节软骨、骨组织损伤、滑膜增生和慢性炎症、血管翳形成为主要病理表现的慢性自身免疫性关节疾病[1].患者常出现关节疼痛、畸形甚至功能丧失进而导致严重的残疾,影响全球约1％的人口,女性发病多于男性,是男性发病率的3倍左右[2].其发病过程非常复杂,目前尚未被阐明,主要与遗传因素、环境因素、免疫细胞、细胞因子、自身抗体等密切相关.正清风痛宁的主要成分是青藤碱.现代药理研究表明,青藤碱具有消炎镇痛、免疫抑制、抗肿瘤等药理作用[3],临床上常用于RA、自身免疫性疾病及肿瘤等多种疾病的治疗.近年来,正清风痛宁在治疗类风湿关节炎方面显示出其独特的潜力和优势[4].现将正清风痛宁治疗类风湿关节炎的临床应用及机理研究综述如下.

The activation of hepatic stellate cells (HSCs) has proved to be pivotal in hepatic fibrosis. Therefore, the suppression of HSC activation is an effective anti-fibrotic strategy. Although studies have indicated that eupatilin, a bioactive flavone found in Artemisia argyi, has anti-fibrotic properties, the effect of eupatilin on hepatic fibrosis is currently unclear. In this study, we used the human hepatic stellate cell line LX-2 and the classical CCl4-induced hepatic fibrosis mouse model for in vitro and vivo experiments. We found that eupatilin significantly repressed the levels of the fibrotic markers COL1α1 and α-SMA, as well as other collagens in LX-2 cells. Meanwhile, eupatilin markedly inhibited LX-2 cell proliferation, as verified by the reduced cell viability and down-regulation of c-Myc, cyclinB1, cyclinD1, and CDK6. Additionally, eupatilin decreased the level of PAI-1 in a dose-dependent manner, and knockdown of PAI-1 using PAI-1-specific shRNA significantly suppressed the levels of COL1α1, α-SMA, and the epithelial–mesenchymal transition (EMT) marker N-cadherin in LX-2 cells. Western blotting indicated that eupatilin reduced the protein level of β-catenin and its nuclear translocation, while the transcript level of β-catenin was not affected in LX-2 cells. Furthermore, analysis of histopathological changes in the liver and markers of liver function and fibrosis revealed that hepatic fibrosis in CCl4-treated mice was markedly alleviated by eupatilin. In conclusion, eupatilin ameliorates hepatic fibrosis and hepatic stellate cell activation by suppressing the β-catenin/PAI-1 pathway.

类风湿关节炎(Rheumatoid Arthritis,RA)是一种以侵蚀性、对称性多关节炎为主要表现的全身性自身免疫性疾病,表现为关节滑膜的慢性炎症、增生、血管翳的形成,随着病程进展逐渐造成骨与软骨的破坏,导致关节畸形、功能丧失.在RA的患病人群中,病程长短与致残率呈正比,老年患者数量也逐渐增多,其中肝肾不足型患者较其他证型占比较大[1].相关指南推荐在RA早期即联合中医药治疗,可以起到增效减毒的作用[2].本研究将中药(包括单味药、药对、汤药、复方中成药)等治疗RA的作用机制研究进展综述如下.

中医要自强,教育需先行.中医药既在抗击新型冠状病毒肺炎(简称"新冠肺炎")疫情的过程中发挥了重要作用,同时也暴露出诸多亟需解决的问题.中医药教育如何应对新冠肺炎疫情引发医学教育的新形势、新要求是中医药教育工作者应当思考的问题.文章立足于新冠肺炎疫情背景,反思和总结中医药教育当前存在的问题,有针对性地从教育模式、师资培养、学科建设、中医药管理及评价体制等方面提出改革的对策和建议,并对中医药教育发展前景进行了预测,以期为我国中医药教育事业改革和发展提供参考.

Green formulated silver nanoparticles offer a great promise in biomedicine. Administration of streptozotocin causes severe hepatotoxicity and nephrotoxicity by increasing the blood glucose. The development of nephroprotective drugs through eco-friendly production routes is a major challenge for current pharmacology and nanotechnology. The creation of cutting-edge technology for the synthesis of effective nephroprotective agents is crucial on a global scale. So in the current study, we report herein the bio-inspired proficient preparation of silver NPs over Pistacia atlantica (P.a.) aqueous extract as natural reducing/capping and stabilizing agent (P.a./Ag NPs) under ultrasonic irradiation. The final hybrid nanocomposite was thereafter characterized by a range advanced analytical methods like, FE-SEM, ICP-OES, EDX, TEM, and elemental mapping. Diabetes was induced by administration of 60 mg/kg of streptozotocin (STZ) intraperitoneally in 100 mature male mice and they were randomly divided into 5 groups. The negative control group received normal saline and treatment groups received glibenclamide with dose 0.5 mg/kg and 10 and 40 mu g/kg of P.a./Ag nanocomposite through gavage for 50 days. On the last day, serum levels of samples blood glucose, urea and creatinine were measured. After tissue processing, 5 mu m sections of the kidneys were prepared and they were stained by periodic acid Schiff (PAS) and used for stereological analysis. The kidney weight, kidney volume (Volume of cortex, medulla, glomerulus, proximal and distal tubules, collecting ducts, loop of Henle, interstitial tissues, and vessels) and kidney structures length (length of proximal and distal tubules, collecting ducts, loop of Henle, and vessels) decreased significantly (p <= 0.05) after treatment with high dose of P.a./Ag NPs nanocomposite (p > 0.05). The increased levels of blood glucose and urea were decreased (p <= 0.05) significantly in P.a./Ag nanocomposite-treated groups as compared to the untreated diabetic. This study suggested using from P.a./Ag nanocomposite as an antidiabetic and nephroprotective drug in the developing countries.

Chronic atrophic gastritis（CAG） is a chronic inflammatory digestive disease with the main symptoms of upper and middle abdominal pain, bloating, belching, and acid regurgitation. The theory of qi movement, one of the theories of traditional Chinese medicine（TCM）, is of great significance for explaining the occurrence and progression of diseases. On the basis of the holistic view of TCM and the theory of qi movement, we analyzed the pathogenesis of CAG and inflammationcancer transformation. We believe that the pathogenesis of CAG is complicated with both deficiency and excess and this disease should be treated according to the different syndromes of the patients on the basis of the theory of qi movement. Taking qi imbalance as the core pathogenesis, we analyze the influences of deficiency and excess of different factors on the occurrence of CAG and propose the therapy of regulating qi movement, tonifying deficiency, and reducing excess based on syndrome differentiation, aiming to provide more reference for the TCM treatment of CAG.

Overview: The treatment of chronic renal failure (CRF) with traditional Chinese medicine has attracted much attention, but its mechanism is not clear. Network pharmacology is an effective strategy for exploring the interaction mechanisms between Chinese herbs and diseases, however, it still needs to be validated in cell and/or animal experiments due to its virtual screening characteristics. Herein, the anti-CRF mechanism of the Fushengong decoction (FSGD) was investigated using a dual-dimension network pharmacological strategy combined with in vivo experiment.Methods: The traditional Chinese medicine systems pharmacology (TCMSP) database (https://tcmspw.com) and UHPLC-MS/MS technology were used to identify the effective compounds of FSGD in theory and practice, such as quercetin, formononetin, and pachymic acid. The putative targets of FSGD and CRF were obtained from the Swisstarget prediction platform and the Genecards database, respectively. The common target pathways between FSGD and CRF were got from the dual-dimension network pharmacology analysis, which integrated the cross-common targets from the TCMSP components-Swisstarget-Genecards-Venn platform analysis in theory, and the UHPLC-MS/MS identified effective ingredients-Swisstarget screening, such as TNF and PI3K/AKT. Furthermore, system molecular determinations were used to prove the dual-dimension network pharmacology study through CRF rat models, which were constructed using adenine and treated with FSGD for 4 weeks.Results: A total of 121 and 9 effective compounds were obtained from the TCMSP database and UHPLC-MS/MS, respectively. After dual-dimension network pharmacology analysis, the possible mechanism of PTEN/PI3K/AKT/NF-κB pathway was found for FSGD in CRF. In vivo experiments indicated that FSGD can play a role in protecting renal function and reducing fibrosis by regulating the PTEN/PI3K/AKT/NF-κB pathway. These findings provide a reference for FSGD in CRF.Conclusion: Based on the theoretical and practical dual-dimension network pharmacology analysis for FSGD in CRF, the possible molecular mechanism of PTEN/PI3K/AKT/NF-κB was successfully predicted, and these results were verified by in vivo experiments. In this study, the dual-dimension network pharmacology was used to interpret the key signal pathway for FSGD in CRF, which also proved to be a smart strategy for the study of effective substances and pharmacology in FSGD.

Aim: Vitamin D plays a vital role in Rheumatoid arthritis (RA). However, the mechanism of vitamin D and rheumatism is still unclear. Therefore, a strategy based on network pharmacology and molecular docking was used to explore the mechanism of vitamin D and RA. Methods: The targets of RA were obtained from the GeneCards database and Therapeutic Targets Database, and the targets of vitamin D were obtained from the Drugbank database and STITCH database. Next, overlapping genes were identified by Venny, and further Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and molecular docking analyses were performed. Results: A total of 1,139 targets of RA and 201 targets of vitamin D were obtained. A total of 76 overlapping genes were identified by Venny. The enrichment analysis showed that cell proliferation, immune response, and apoptotic process were the critical biological processes of vitamin D in treating RA. Antifolate resistance, osteoclast differentiation, and the nuclear factor-kappa B (NF-κB) signalling pathway are fundamental mechanisms of vitamin D in treating RA. According to further molecular docking, ALB, TNF, CASP3, and TP53 may be important punctuation points or diagnostic markers for future RA treatment. Conclusion: By analysing overlapping genes of diseases and drugs, this study confirmed that ALB, TNF, CASP3, and TP53 may be essential markers or diagnostic markers for future RA treatment.

The INO80 chromatin remodeling complex plays an essential role in the regulation of gene transcription, which participate in a variety of important biological processes in cells including DNA repair and DNA replication. Difference from the yeast INO80 complex, metazoan INO80 complex have the specific subunit G, which is known as nuclear factor related to kappaB binding protein (NFRKB). Recently, NFRKB has been received much attention in many aspects, such as DNA repair, cell pluripotency, telomere protection, and protein activity regulation. To dig the new function of metazoan INO80 complex, a better understanding of the role of NFRKB is required. In this review, we provide an overview of the structure and function of NFRKB and discuss its potential role in cancer treatment and telomere regulation. Overall, this review provides an important reference for further research of the INO80 complex and NFRKB.