Introduction Hepatic fibrosis is a key reversible stage of chronic liver disease progression, with a lack of effective and specific clinical therapies. Traditional Chinese Medicine formulations show unique advantages. This study aimed to elucidate the multi-target mechanisms of Danggui Biejia Decoction (DGBJD) against hepatic fibrosis using an integrated approach combining network pharmacology and in vitro experimental validation. Methods Network pharmacology was used to screen active components and anti-hepatic fibrosis targets of DGBJD. Molecular docking was performed to verify the binding affinities between core components and hub targets. Experimentally, the anti-proliferative effects of DGBJD on human hepatic stellate cells (LX-2) were assessed using CCK-8 assays. Furthermore, Western blot analysis—incorporating a vehicle-only blank control and Pirfenidone (PFD) as a positive control—was performed to validate the underlying molecular mechanisms in TGF-β1-activated LX-2 cells. Results Network analysis identified 29 core active components (e.g., quercetin, kaempferol) and 194 overlapping disease-drug targets. Molecular docking confirmed stable binding between these key components and core targets, including TGF-β1 and AKT1. In vitro, DGBJD significantly suppressed LX-2 cell proliferation in a concentration- and time-dependent manner. Notably, compared with the TGF-β1 model group, DGBJD exhibited therapeutic efficacy comparable to that of the positive drug PFD, significantly reversing the pathological upregulation of α-SMA, COL1A1, and TNF-α. Mechanistically, DGBJD markedly downregulated the phosphorylation levels of key proteins in the TGF-β/Smad, PI3K/AKT, and NF-κB signaling pathways. Conclusion DGBJD exerts potent anti-hepatic fibrotic effects through a multi-component, multi-target synergistic mechanism. By targeting the TGF-β/Smad, PI3K/AKT, and NF-κB pathways, DGBJD effectively inhibits hepatic stellate cell activation, excessive extracellular matrix deposition, and inflammatory responses, providing a robust scientific basis for its clinical application.

Macrophage-mediated tumor clearance is frequently restricted by the immunosuppressive tumor microenvironment. This study investigates the immunomodulatory effects of plasma-activated medium (PAM) on macrophage pro-inflammatory activation and antitumor function. Murine RAW264.7 and primary bone marrow-derived macrophages were treated with PAM generated by a helium atmospheric pressure plasma jet. Phenotypic changes and underlying signaling mechanisms were assessed. Functional enhancements in macrophage recruitment and tumor engulfment were quantified using chemotaxis and 3D confocal co-culture assays with Panc02 pancreatic cancer cells. Results show that PAM promotes macrophage activation by increasing spatial recruitment via pro-inflammatory chemokine secretion and enhancing tumor cell engulfment. Mechanistically, PAM drives this functional shift through hierarchical activation of the TLR4/NF-κB and PI3K/AKT signaling cascades. Furthermore, while hydrogen peroxide alone triggers a compensatory upregulation of the inhibitory SIRPα receptor, the reactive oxygen and nitrogen species (RONS) in PAM bypass this negative feedback to directly downregulate SIRPα. These findings demonstrate that PAM-mediated oxidative modulation effectively suppresses the “don't-eat-me” signal and enhances innate antitumor immunity, providing a potential strategy for cancer immunotherapy.

The purpose of this study was to investigate the therapeutic effects and underlying mechanisms of Wenyang Huazhuo Formula (WYHZF) extract in diabetic kidney disease (DKD) in db/db mice. DKD mice were administered WYHZF extract by oral gavage, and glycolipid metabolism, renal function, and renal pathology were assessed. Renal histopathology was evaluated using H&E, PAS, and Masson’s trichrome staining. UPLC-QE-Orbitrap-MS, HPLC, and UV-Vis spectroscopy were employed to characterize prototype and potential blood-absorbed metabolites of WYHZF extract. Renal RNA-seq was conducted to identify differentially expressed genes and related pathways. Molecular docking and molecular dynamics simulations were used as supportive in silico analyses to assess the plausibility of interactions between representative metabolites and H2-Aa/H2-Ab1. Western blotting (WB) was performed to validate H2-Aa and H2-Ab1 regulation and to examine fibrosis-associated proteins TGF-β and α-SMA. Gut microbiota alterations were evaluated by 16S rRNA sequencing. WYHZF extract significantly improved hyperglycemia and dyslipidemia, reduced UACR, serum creatinine, and BUN, alleviated glomerular/tubular injury, and restored Nephrin and NGAL expression. Transcriptomic analysis indicated aberrant activation of MHC class II–related pathways in DKD kidneys, which was modulated after WYHZF treatment. Docking and molecular dynamics simulations suggested compatible binding modes and stable interaction patterns between several representative metabolites and H2-Aa/H2-Ab1 under simulated conditions. WB confirmed that H2-Aa and H2-Ab1 were upregulated in DKD and were reversed by WYHZF; notably, TGF-β and α-SMA were also reduced, consistent with attenuation of renal fibrotic features. In addition, WYHZF partially restored gut microbiota diversity and corrected key taxonomic imbalances. Collectively, WYHZF extract may exert multi-level benefits in DKD, accompanied by modulation of MHC class II-related molecules, reduced fibrosis-associated signals, and gut microbiota remodeling.

Ovarian cancer remains a significant challenge in oncology due to its aggressive nature, late-stage diagnosis, and high rates of chemoresistance, particularly to platinum-based therapies like cisplatin. The epithelial-mesenchymal transition (EMT) is a key driver of ovarian cancer metastasis and drug resistance, highlighting the need for novel therapeutic strategies. Cold atmospheric plasma (CAP) and plasma-activated liquids (PAL), including plasma-activated medium (PAM) and saline (PAS), have emerged as promising anticancer agents, generating reactive oxygen and nitrogen species (RONS) that selectively target cancer cells. This study investigates the potential of PAL to inhibit the invasion and metastasis of cisplatin-resistant ovarian cancer cells and explores its synergistic effects with cisplatin. In vitro, PAM reduced proliferation, migration, and invasion of cisplatin-resistant ovarian cancer cells (A2780/DDP and SKOV3/DDP) while downregulating EMT-related proteins (N-cadherin, β-catenin, vimentin). H2O2 in PAM inhibit the PI3K/AKT/GSK3β pathway, promoting degradation of EMT regulators Snail, Slug, and β-catenin. Combining PAM with cisplatin enhanced therapeutic efficacy, reducing cell viability and metastatic potential. In vivo studies using an orthotopic mouse model further confirmed that PAS combined with low-dose cisplatin effectively suppressed tumor growth and metastasis with minimal side effects. These findings underscore the potential of PAL as an adjuvant therapy for cisplatin-resistant ovarian cancer, offering a novel approach to overcome drug resistance and inhibit metastasis. Future research should focus on optimizing treatment protocols and elucidating the molecular mechanisms underlying the synergistic effects of PAL and cisplatin.

Background Metformin, widely used for type 2 diabetes, raises concerns about its use in chronic kidney disease (CKD) due to risks like lactic acidosis and renal function impact. This study uses Mendelian randomization (MR) and summary data-based MR (SMR) to explore metformin’s potential causal relationship with CKD and associated genes.Methods We employed MR methods (MR-Egger, weighted median, IVW) and sensitivity analyses to explore the causal relationship between metformin and CKD. SMR was used to analyze eQTL and CKD data from the UK Biobank and FinnGen, intersecting these with metformin drug targets to identify genes associated with CKD.Results MR analysis indicated that metformin may increase CKD risk (IVW model: OR = 144.67, p < 0.01). However, given the high OR value, additional studies are warranted to validate this finding. SMR identified genes ANPEP, STK11, ACACB, and RPS6KB as significantly associated with CKD risk.Conclusion The study suggests metformin could elevate CKD risk and identifies relevant genes. Clinicians should exercise caution when prescribing metformin, particularly for patients with renal issues. Further research is needed to confirm these findings and guide clinical practices.

BACKGROUND:Curcumin has been shown to inhibit renal fibrosis, but whether curcumin mediates renal fibrosis progression by regulating the circular RNA (circRNA)-related pathway remain unclear. METHODS:TGF-β1 was used to construct renal injury and fibrosis cell model. Cell growth was evaluated by cell counting kit 8 assay, EdU assay and flow cytometry. Fibrosis marker and interleukin 6 signal transducer (IL6ST) protein levels were measured using western bolt analysis. Inflammation factor concentrations were determined by ELISA. Circ_0008925, miR-204-5p and IL6ST expression was assessed by qRT-PCR. Unilateral ureteral obstruction (UUO) mice models were constructed to assess the role of curcumin in vivo. RESULTS:Curcumin treatment alleviated TGF-β1-induced HK-2 cell apoptosis, inflammation and fibrosis in vitro, as well as relieved renal injury in UUO mice models in vivo. Circ_0008925 was highly expressed in TGF-β1-induced HK-2 cells and its expression was inhibited by curcumin. Circ_0008925 could sponge miR-204-5p to positively regulate IL6ST. The inhibition effect of curcumin on TGF-β1-induced HK-2 cell injury and fibrosis was reversed by circ_0008925 overexpression, miR-204-5p inhibitor or IL6ST upregulation. Besides, circ_0008925 knockdown inhibited TGF-β1-induced HK-2 cell injury and fibrosis by suppressing IL6ST expression. CONCLUSION:Curcumin relieved renal fibrosis through regulating circ_0008925/miR-204-5p/IL6ST axis.

BackgroundPost-COVID sequelae include skin abnormalities with nonspecific characteristics, making disease-specific diagnosis challenging. Conventional treatment primarily relies on modern medical approaches, and the potential of complementary therapies, such as acupuncture, remains underexplored.Case reportThis case describes a patient who developed abnormal skin pigmentation following a COVID-19 infection and was initially diagnosed with five different conditions. After a prolonged period of unsuccessful treatment with conventional medicine, the patient received complementary therapy, leading to significant symptom improvement.ConclusionComplementary therapies, such as acupuncture, may prove beneficial in treating skin conditions that lack a definitive diagnosis, as demonstrated in this case.

BackgroundKidney transplant recipients (KTRs) are at an increased risk of osteoporosis, which negatively impacts their quality of life and transplant outcomes. However, the efficacy and safety of anti-osteoporosis treatments in this group remain uncertain.MethodsWe conducted a systematic search of PubMed, Embase, Web of Science, and the Cochrane Central Register of Controlled Trials up to August 1, 2024. Randomized controlled trials (RCTs) examining anti-osteoporotic medications in KTRs were included. Primary outcomes were changes in bone mineral density (BMD) at femoral neck and lumbar spine, and adverse events. We performed a frequentist network meta-analysis using random-effects models. Evidence certainty was assessed using the GRADE approach.ResultsTwenty-one RCTs involving 1,066 participants were included, published between 2000 and 2021. For femoral neck BMD, bisphosphonates significantly improved BMD compared to control (MD = 0.04, 95%CI=0.00-0.09, p<0.05) based on low certainty evidence, while calcitonin was significantly superior to calcium (MD=-0.14, 95%CI=-0.28 to -0.01). Most other comparisons showed no statistically significant differences based on very low to moderate certainty evidence. For lumbar spine BMD, bisphosphonates, calcitonin, and calcium demonstrated statistically significant inferiority compared to denosumab, with bisphosphonates showing MD=-4.98 (95%CI=-6.84 to -3.13), calcitonin showing MD=-4.35 (95%CI=-6.24 to -2.47), and calcium showing MD=-5.85 (95%CI=-7.72 to -3.98), while denosumab was superior to control (MD = 5.10, 95%CI=3.25-6.95), based on low to very low certainty evidence from one RCT. Calcitonin was also significantly superior to calcium (MD = 0.60, 95%CI=0.07-1.12). For safety outcomes, no statistically significant differences were observed between interventions based on low to moderate certainty evidence.ConclusionDenosumab appears most effective for improving lumbar spine BMD in KTRs, while calcitonin shows promise for femoral neck BMD improvement. However, the low to moderate certainty of evidence necessitates individualized treatment approaches considering patient-specific factors including renal function and safety profiles. These findings suggest current guidelines emphasizing bisphosphonates as first-line therapy may require revision, though larger long-term studies with fracture endpoints are needed to confirm these results.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/?utm_source=chatgpt.com, identifier PROSPERO CRD42024587203.

Since the antitumor effect of low-temperature plasma (LTP) was first discovered in 2007, efforts have been devoted to investigating its therapeutic effects in various tumors. LTP has been shown to induce diverse cell death pathways in a dose-dependent manner, modulate immunogenic responses, and suppress tumor invasion and metastasis. However, the precise mechanisms underlying these effects remain poorly elucidated. In this study, we investigated the role of LTP in melanoma growth inhibition. Our findings demonstrate that LTP suppresses melanoma progression by enhancing T-cell-mediated immunity. Mechanistic investigations suggest that direct LTP treatment modulates cytokine expression in regulatory T cells (Tregs) and CD8(+) T cells, while indirect LTP treatment regulates cytokine levels and inhibits the signal transducer and activator of transcription 3 (STAT3) signaling pathway, contributing to its antitumor activity. These results not only provide a potential novel strategy for melanoma treatment but also advance our understanding of the interplay between LTP and the immune system.

Background Chronic Kidney Disease (CKD) is a progressive condition characterized by a decline in kidney function and structural damage, often leading to severe health outcomes. The kidneys are crucial in maintaining homeostasis, including fluid and electrolyte balance, acid-base regulation, and waste excretion. CKD affects millions worldwide, with many individuals unaware of their condition due to subtle early symptoms. Current treatments primarily delay disease progression, highlighting the need for innovative therapeutic strategies. Programmed cell death (PCD), involving mechanisms such as apoptosis and necroptosis, significantly contributes to CKD progression. Purpose Traditional Chinese Medicine (TCM), particularly Zhenwu Decoction, offers a multi-target approach that may alleviate CKD symptoms. The current study was designed to elucidate the mechanisms by which Zhenwu Decoction affects CKD progression and to validate its potential as a novel therapeutic option using bioinformatics and network pharmacology. Materials and Methods Zhenwu Decoction, composed of aconite, Poria, Atractylodes macrocephala, white peony root, and ginger, was prepared by dissolving the granules in distilled water. The decoction was administered to rats at a specified dosage based on body weight. Aconite and the pharmaceutical telmisartan were also prepared and administered to evaluate their effects comparatively. The study utilized 40 Sprague-Dawley rats, divided equally by sex, to model doxorubicin-induced nephropathy. Rats were housed under controlled conditions, with daily monitoring of their health and behavior. Rats received a single tail vein injection of doxorubicin to induce nephropathy, with a control group receiving saline. Successful modeling was confirmed by observing physical symptoms and elevated urine protein levels. Rats were treated with Zhenwu Decoction, aconite, or telmisartan. The effects of these treatments on nephropathy symptoms and kidney function were assessed. Kidney tissues were analyzed using Hematoxylin and Eosin (HE) staining for morphology, Masson’s Trichrome staining for fibrosis, and PASM staining for structural visualization. The study included analyzing the expression of the rapamycin target protein mTOR, with protein extraction performed on kidney samples post-treatment. Results Our results show that Zhenwu Decoction (ZWD) effectively treats CKD by reducing symptoms, proteinuria, and kidney damage. Its efficacy stems from a multi-targeted approach, simultaneously modulating inflammation, fibrosis, and programmed cell death (PCD). ZWD significantly reduces fibrotic markers like TIMP3 and Col-IV, influencing ECM-receptor interaction and TGF-β signaling. It also modulates inflammation through the NF-$\kappa$B pathway and mTOR/autophagy axis, downregulating pro-inflammatory cytokines while increasing anti-inflammatory ones. Furthermore, ZWD regulates PCD by decreasing necroptosis markers and inhibiting ferroptosis via ALOX12 reduction, while upregulating anti-apoptotic PARP2 for enhanced DNA repair. This comprehensive action across various pathways provides superior renal protection. Despite the documented efficacy of Zhenwu Decoction (ZWD) in clinical practice, a significant gap remains in systematically integrating bioinformatics predictions with experimental validation to elucidate its multi-target mechanisms against programmed cell death (PCD) in CKD. This study was therefore designed to bridge this gap by employing a comprehensive network pharmacology approach alongside in vivo validation to definitively map ZWD's reno-protective actions onto specific inflammatory, fibrotic, and PCD pathways, thereby providing a mechanistic foundation for its therapeutic application. Conclusions Our present study shows the potential of Zhenwu Decoction in the management of chronic kidney disease using a bioinformatics and network pharmacology strategy to target kidney function and programmed cell death. Its active components advanced our knowledge of TCM's multi-target effects by improving kidney health in a rat model of doxorubicin-induced nephropathy.

Cisplatin resistance coupled with adverse effects presents substantial hurdles in the treatment of ovarian cancer. Both cold atmospheric plasma and plasma-activated liquid (PAL) hold the ability to induce DNA damage, which is a primary target of cisplatin. In this study, we investigate the potential of PAL in augmenting cisplatin sensitivity or diminishing the necessary drug dosage by impairing the DNA of cisplatin-resistant cancer cells. We found that plasma irradiated medium exceeding 40 s could decrease the viability, induce DNA damage, trigger cell cycle arrest, and augment apoptosis and autophagy in two types of cisplatin-resistant ovarian cancer cells (A2780/DDP and SKOV3/DDP) after a 24 h incubation period. Notably, pre-treatment with 40 s plasma-activated medium (PAM) for 2 h significantly enhanced the anti-cancer effect of cisplatin administered at lower doses on these cell types. RNA-seq, quantitative real-time PCR and Western blotting analysis revealed that PAM treatment could downregulate the expression of several pivotal proteins involved in nucleotide excision repair (NER) and homologous recombination repair (HRR). The mouse xenograft tumor model demonstrated that plasma-activated saline and cisplatin synergistically inhibited tumor growth and significantly suppressed the expression of proteins related to HRR and NER pathways. We identified plasma-derived peroxide generation in PAM as crucial in these processes. These results pave the way for considering PAM as an adjuvant treatment for cisplatin-resistant ovarian cancer and other abdominal cancers. Additionally, the findings indicate the feasibility of reducing cisplatin dosage to alleviate side effects through sensitization.

IntroductionUlcerative colitis (UC) and diabetic kidney disease (DKD) are chronic disorders with multifaceted pathogenesis, posing significant challenges in clinical management. While substantial efforts have been made to investigate the individual causes of these diseases, the interplay between UC and DKD is not well understood. This study aims to elucidate the genetic association between UC and DKD through Mendelian randomization (MR) analysis, offering new insights into common biological pathways and potential clinical implications.MethodsWe conducted a bidirectional two-sample MR study utilizing data from large-scale genome-wide association studies (GWAS) for both UC and DKD. Instrumental variables (IVs) were meticulously selected according to genome-wide significance and stringent statistical criteria, ensuring robust causal inference. Various MR methodologies, including inverse variance weighting (IVW), were employed to assess the causal relationships between UC and DKD. Sensitivity analyses were also performed to validate the robustness of our findings.ResultsOur analysis revealed a significant causal relationship between genetic predisposition to UC and increased susceptibility to DKD. Specifically, individuals with a genetic susceptibility to UC exhibited a 17.3% higher risk of developing DKD. However, we found no evidence of a causal link between DKD and the risk of developing UC. Additionally, we identified shared genetic risk factors and molecular pathways linking UC and DKD, thereby highlighting potential therapeutic targets.DiscussionThis study underscores the intricate genetic interplay between UC and DKD, suggesting that individuals with UC may be at an elevated risk for developing DKD. Understanding these shared genetic pathways could facilitate the development of early detection strategies and targeted interventions for individuals at risk of DKD. Ultimately, these insights could lead to improved clinical outcomes for patients suffering from both conditions.

Abstract Immunotherapy is effective in the treatment of melanoma due to its immunogenicity. In recent years, researchers have identified LTP is rich in active substances that can induce apoptosis in tumor cells and trigger an immune response. However, it is unclear how LTP works to antitumor by enhancing immune cell function. Therefore, the purpose of this study is to investigate the effects of direct and indirect LTP treatments on the quantity and function of Treg cells and CD8+ T cells in B16-F10 melanoma-bearing mice and their associated mechanisms. The results revealed that both direct and indirect LTP treatments were effective at inhibiting tumor growth and extending the survival of B16-F10 melanoma-bearing mice. In addition, both direct and indirect LTP treatments reduced the number of Treg cells and improved the immune function of CD8+ T cells in the spleen and tumor. Nevertheless, the indirect LTP treatment proved to be more effective than the LTP direct treatment. Mechanistic studies demonstrated that direct LTP treatment might affect the quantity and function of Treg cells and CD8+ T cells by modulating cytokine level changes. However, indirect LTP treatment might have a greater tumor immunotherapeutic potential by inhibiting the activation of key protein molecules in the IL-6/STAT3 signaling pathway and regulating cytokine level changes. In conclusion, this study reveals that LTP exerts an anti-melanoma effect by regulating the level and function of Treg cells and CD8+ T cells. This study is expected to provide new ideas for LTP anti-tumor immunotherapy.

"育人为本、德育为先"是实施高校教育的主导思想,中医药文化是博大精深的中华文化的瑰宝,在西医院校中的中医课程作为中医文化传承的重要载体和中医文化创新的重要源泉,将其融入西医院校的中医课程教学中,不仅丰富了西医院校中医课程的教学内容,加强了课程思政建设,也是传承中华民族文化的必然选择.本文分析高校专业课程思政教学中目前存在的主要问题,其中包括对课程思政主体认识不够;高校课程思政缺乏创新,立德树人成效不显;社会价值的多元化,加大了立德树人教育目标实现难度;课程评价体系中德育权重较小,影响立德树人目标的实现等.并围绕如何实现中医专业课程教学过程中的育人内涵展开讨论,可通过运用多种形式,挖掘中医文化的立德育人资源和内涵;提升专业课授课教师队伍的人文素质;通过设计调查问卷及多方评价不断改进与完善教学方法;充分利用线上课程及网络空间的优势,弥补课堂教学的不足等,从而探索出适合西医院校中医课程思政教学的特色课堂模式,达到将专业知识与课程思政内容紧密融合,引导学生实现中医人文知识的内化和道德情操的升华.

Mesangial proliferative glomerulonephritis (MesPGN) is a common renal disease that lacks effective drug intervention. Aconiti Lateralis Radix (Fuzi), a natural Chinese medical herb, is found with significant therapeutic effects on various diseases in the clinic. However, its effects on MesPGN have not been reported. This study is aimed to discuss the therapeutic effects of the aqueous extract of Aconiti Lateralis Radix (ALR) and the polysaccharides of Aconiti Lateralis Radix (PALR) on MesPGN as well as the underlying mechanism. In this study, we, firstly, studied the anti-MesPGN mechanism of ALR and PALR. ALR and PALR inhibit the proliferation of the mesangial cells through the PI3K/AKT/mTOR pathway, induce the G0/G1 phase of block and apoptosis, inhibit the activity of Cyclin E and CDK2, increase the expression of Bax, cleaved caspase-8/caspase-8, and cleaved caspase-3/caspase-3 proteins, and effectively inhibit the growth of the mesangial cells. Overall, our data suggest that ALR and PALR may be potential candidates for MesPGN and that PALR is more effective than ALR.

PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) have been proved to be hazardous to health. Previous studies have focused on the distribution and sources of PAHs, whereas there is little knowledge of the damage to organs. Here we sought to investigate the pollution level and seasonal variation characteristics of PAHs in PM2.5 in Xi'an and assess the health risk, to establish a PAHs exposure model, and investigate the toxicological effects of PAHs on the respiratory and immune functions. A sub-chronic exposure model of PAHs was established by inhalation. The pathological changes of lung tissues were observed with a light microscope. Inflammatory reactions in alveolar lavage fluid were determined using the corresponding kit. The levels of interleukin-6 (IL-6) and interleukin-8 (IL-8) were detected with enzyme linked immunosorbent assay (ELISA) kit; the proliferation of lymphocytes in spleen was detected with methyl tetrazolium (MTT); DNA immune damage was determined with DNA gel electrophoresis. The results showed that (1) the total concentration of 16 PAHs ranged from 41.1 to 387 ng/m(3), with a mean value of 170 ng/m(3), and the concentration of PAHs in PM2.5 was higher in winter than in other seasons. (2) The sources of PAHs in the atmosphere of Xi'an urban area were mainly coal combustion, and the equivalent carcinogenic concentration of PAHs in PM2.5 was 3.9 ng/m(3). (3) Foreign body granuloma formation and inflammatory cell damage were observed in the lungs of rats infected with toxin; the levels of reactive oxygen species (ROS) and mobile device assistant (MDA) increased while nitric oxide synthase (NOS) decreased with the increase of dose; the expression levels of IL-6 and IL-8 elevated with the increase of toxin dose, showing an obvious dose-effect relationship; the level of PAHs damage to cells showed a dose-effect relationship. Sub-chronic exposure to PAHs could cause sustained inflammatory injury to the organism. Measures should be taken to counter the problems of PAHs in PM2.5 in Xi'an and relevant health promotion strategies should be developed.

乔成林教授认为肾囊肿因阳虚血瘀、痰瘀互阻而致,以"治水必先温通"学术思想为指导,立"温阳活血"之法,创"温阳活血"方,疗效显著,为临床肾囊肿的治疗提供了参考.

目的 探讨针刺运动疗法、温针灸结合康复治疗改善中风后患侧上肢肌痉挛的临床疗效.方法 将60例中风后上肢肌痉挛的患者按随机数字表法分为对照组与治疗组.对照组以常规针刺和康复治疗;治疗组给予温针灸、针刺运动疗法和康复治疗,观察两组患者治疗前后患侧上肢肌痉挛程度改善情况,比较两组患者治疗前后MAS、FMMS、ADL评分.结果 经治疗,治疗组总有效率为90％,对照组总有效率为80％,差异有统计学意义(P＜0.05);治疗后,两组患者患侧上肢痉挛程度、MAS、FMMS、ADL量表评分较治疗前均有改善,且治疗组疗效明显高于对照组(P＜0.05).结论 针刺运动疗法、温针灸结合康复治疗能有效降低中风患者患侧上肢肌张力,改善肢体运动功能,促进日常生活能力的恢复.

交感神经为能量消耗型活动神经,副交感神经为保存恢复能量型神经,与中医认为的阴阳活动类似.自主神经系统可视为人体阴阳表现的物质基础.失眠产生的重要机制为交感神经过度兴奋、副交感神经兴奋性降低.针刺对于自主神经功能具有双向、良性的调整作用,能够使之恢复平衡.治疗失眠最常选用的穴位有神门、三阴交、印堂、百会等.神门为手少阴心经原穴,三阴交属于足太阴脾经,且为三条阴经(足太阴脾经、足少阴肾经、足厥阴肝经)的交会穴,二者均与阴经联系密切;印堂与百会穴则属于督脉穴位,与阳经紧密关联,故针刺上述穴位能够调整阴阳平衡,阴平阳秘则心神自安.

One of the hallmarks of placental dysfunction is the increase of oxidative stress. This process, along with the overexpression of the inflammasome, creates a downward spiral that can lead to a series of severe pregnancy complications. Ferroptosis is a form of iron-mediated cell death involving the accumulation of reactive oxygen species, lipid peroxides. In this study, the rats’ model of oxidative stress abortion was established, and hydrogen peroxide (H2O2) was used to establish a cellular model of placental oxidative stress. RNAi, western blot, and immunofluorescence were used to evaluate the expression of specific markers of ferroptosis and the expression of the inflammasome in placental trophoblast cells. We observed excessive levels of ferroptosis and inflammasome activation in both rats’ model and placental trophoblast cell model of oxidative stress. When the NLRP1 inflammasome was silenced, the expression levels of GSH and Glutathione peroxidase 4 (GPX4) were increased, while the expression levels of transferrin receptor 1 (TFR1), acyl-CoA synthetase long-chain family member 4 (ACSL4), Superoxide dismutase (SOD), and Malondialdehyde (MDA) were decreased. However, when an NLRP1 activator was applied, we observed the opposite phenomenon. We further explored the mechanisms underlying the actions of ferroptosis to inflammasomes. The expression levels of NLRP1, NLRP3, IL-1β, and caspase-1 were positively correlated with the ferroptosis following the application of ferroptosis inhibitor (ferrostatin-1) and ferroptosis activator (erastin). The existence of ferroptosis was demonstrated in the oxidative stress model of placental trophoblast cells; the results also indicate ferroptosis is linked with the expression of NLRP1 inflammasome. These findings may provide a valuable therapeutic target for the pathogenesis of pregnancy-related diseases.