STATEMENT OF PROBLEM:Although digitally fabricated complete dentures have developed rapidly and have demonstrated significant application potential, systematic reviews on their current research status, technical challenges, and clinical applications are lacking. PURPOSE:The purpose of this systematic review was to evaluate current research advancements and identify critical technical bottlenecks in digitally fabricated complete dentures while providing evidence-based guidance for clinical implementation. MATERIAL AND METHODS:An electronic search was conducted across PubMed/MEDLINE, Embase, and Web of Science databases to identify studies published between January 2000 and December 2024. Following a dual independent screening process with conflict resolution, data extraction was systematically conducted on digital workflow protocols, material specifications, clinical efficacy metrics, and procedure-related complications. RESULTS:An analysis of the 21 included studies revealed that 3 studies explored the clinical workflows and laboratory technical details of digitally fabricated complete dentures, 4 studies focused on current technological or application challenges faced by them, 1 study systematically evaluated advancements in materials research for digitally fabricated complete dentures, and 2 studies provided in-depth analyses of the technical features of computer-aided design and computer-aided manufacture (CAD-CAM) software programs and scanning devices. In terms of performance comparisons, 6 studies experimentally compared morphological differences in the tissue surface of denture bases between digital and conventional methods, and 2 studies quantitatively analyzed their retention and stability. Seven studies conducted empirical comparisons of clinical outcomes (such as patient comfort and functional recovery) between digitally fabricated and conventionally fabricated complete dentures. CONCLUSIONS:While digitally fabricated complete dentures show great potential, further research and improvement are needed to overcome existing obstacles.

Wound healing impairment in diabetes mellitus is associated with an excessive inflammatory response and defective regeneration capability with suppressed Hedgehog (Hh) signaling. The bromodomain protein BRD9, a subunit of the non-canonical BAF chromatin-remodeling complex, is critical for macrophage inflammatory response. However, whether the epigenetic drug BRD9 degrader can attenuate the sustained inflammatory state of wounds in diabetes remains unclear. Without a bona fide immune microenvironment, Hh signaling activation fails to effectively rescue the suppressed proliferative ability of dermal fibroblasts and the vascularization of endothelial cells. Therefore, a silk-based core-shell microneedle (MN) patch is proposed to dynamically modulate the wound immune microenvironment and the regeneration process. Specifically, the BRD9 degrader released from the shell of the MNs mitigated the excessive inflammatory response in the early phase. Subsequently, the positively charged Hh signaling agonist is released from the negatively charged core of the silk fibroin nanofibers and promotes the phase transition from inflammation to regeneration, including re-epithelialization, collagen deposition, and angiogenesis. These findings suggest that the programmed silk-based core-shell MN patch is an ideal therapeutic strategy for effective skin regeneration in diabetic wounds.

Chromatin remodeler ARID1A regulates gene transcription by modulating nucleosome positioning and chromatin accessibility. While ARID1A-mediated stage and lineage-restricted gene regulation during cell fate canalization remains unresolved. Using osteoclastogenesis as a model, we show that ARID1A transcriptionally safeguards the osteoclast (OC) fate canalization during proliferation-differentiation switching at single-cell resolution. Notably, ARID1A is indispensable for the transcriptional apparatus condensates formation with coactivator BRD4/lineage-specifying transcription factor (TF) PU.1 at Nfatc1 super-enhancer during safeguarding the OC fate canalization. Besides, the antagonist function between ARID1A-cBAF and BRD9-ncBAF complex during osteoclastogenesis has been validated with in vitro assay and compound mutant mouse model. Furthermore, the antagonistic function of ARID1A-"accelerator" and BRD9-"brake" both depend on coactivator BRD4-"clutch" during osteoclastogenesis. Overall, these results uncover sophisticated cooperation between chromatin remodeler ARID1A, coactivator, and lineage-specifying TF at super-enhancer of lineage master TF in a condensate manner, and antagonist between distinct BAF complexes in the proper and balanced cell fate canalization.

Clinically amyopathic dermatomyositis (CADM) is characterized by typical skin lesions with no (amyopathic) or subclinical (hypomyopathic) evidence of muscle involvement. Patients with CADM may also develop rapidly progressive interstitial lung disease (ILD), and have a poor prognosis. However, the diagnosis of rapidly progressive ILD faces a challenge during the severe acute respiratory syndrome coronavirus 2 pandemic. Severe acute respiratory syndrome and ground-glass attenuation on a chest computed tomography scan are the presenting features in both conditions. A 45-year-old woman with amyopathic dermatomyositis had acute onset of fever and dyspnea in February 2020. She had abnormal lung findings on CT scan. Polymerase chain reaction testing for SARS-CoV-2 was not available at that time. Chest CT revealed non-specific manifestations that could be either the signs of ILD or SARS-CoV-2 infection. Antiviral therapy was initiated with oseltamivir. Three days later, she had erythema on face, palm, and back. The ratio of lactate dehydrogenase (LDH) isoenzyme 3 to total LDH was elevated. The ratio of LDH isoenzyme 1 to total LDH was declined. Therefore, she was transferred to the rheumatology ward for further treatment. However, she died from respiratory failure 2 weeks later. We speculate that the altered LDH isoenzyme pattern may be an early biomarker for co-occurrence of CADM and ILD.

Critical-size bone defect repair is in high demand but is difficult to treat. Modern therapies, such as autograft and cell-based treatments, face limitations, including potential immunological rejection and tumorigenesis. Therefore, extracellular vesicle (EV)-based strategies have been proposed as a novel approach for tissue regeneration owing to EVs' complex composition of lipids, proteins, and nucleic acids, as well as their low immunogenicity and congenital cell-targeting features. Despite these remarkable features of EVs, biomimetic synthesis and optimization of natural EVs can lead to enhanced bioactivity, increased cellular uptake, and specific cell targeting, aiming to achieve optimal therapeutic efficacy. To maximize their function, these nanoparticles can be integrated into bone graft biomaterials for superior bone regeneration. Herein, we summarize the role of naturally occurring EVs from distinct cell types in bone regeneration, the current strategies for optimizing biomimetic synthetic EVs in bone regeneration, and discuss the recent advances in applying bone graft biomaterials for the delivery of EVs to bone defect repair. We focused on distinct strategies for optimizing EVs with different functions and the most recent research on achieving time-controlled release of nanoparticles from EV-loaded biomaterials. Furthermore, we thoroughly discuss several current challenges and proposed solutions, aiming to provide insight into current progress, inspiration for future development directions, and incentives for clinical application in this field.

After grinding Trypanosoma brucei with alumina or silicon carbide, it is possible to prepare a multienzyme complex which catalyses the breakdown of glucose to l-glycerol-3-phosphate and 3-phosphoglycerate. The complex sediments with the postnuclear large granule fraction which pellets at 14,500g; it is also eluted in the void volume during Bio-Gel A-5m column chromatography of a cell homogenate. During isopycnic sucrose gradient centrifugation, the multienzyme complex bands at a density of 1.22 g/ml. Because this is the density of T. brucei microbodies, and because Triton X-100 treatment of the material greatly enhances the activities of its component enzymes, we conclude that the multienzyme complex is probably located in the microbodies of the bloodstream long slender forms of T. brucei.

Objectives: To demonstrate the clinicopathological and radiological features of orthokeratinized odontogenic cysts (OOCs), and analyze the epithelial cell proliferative activity between OOCs and odontogenic keratocysts (OKCs). Materials and methods: Clinicopathological and radiological analyses were performed in all OOC cases. The expression of cell proliferation markers, Ki-67 and cyclin D1, was detected by immunohistochemistry. Results: A total of 48 OOC patients, 28 males and 20 females, were included. The mean age was 33.50 years, with a range of 13-61 years. The mandible was affected five times as frequently as the maxilla (mandible 40, maxilla 8). All OOCs were unilocular radiolucencies with well-defined margins, and 30 of 36 showed loss of continuity of the buccal or lingual cortices based on computed tomography (CT) images. Three cases exhibited root resorption; tooth displacement occurred in 4 cases. The average volume of the cysts on CT was 7794.25 +/- 6952.98 mm3. All cysts were treated by enucleation or enucleation after decompression. The average follow-up time was 32.50 +/- 27.58 months (ranging from 6 to 65 months), and the overall recurrence rate was 4.44% (2 of 45). Compared with OKCs, Ki-67 and cyclin D1 expression were significantly lower in OOCs (P < 0.001). Conclusions: OOCs occur more frequently in mandible with a slight male predilection and have a lower proliferative activity than OKCs. Radiologically, OOCs are more likely associated with buccolingual expansion and destruction of cortical bone. Due to the lower aggressiveness and recurrence rate, enucleation or decompression combined with enucleation is the first treatment choice for OOC.

OBJECTIVE:To analyze the clinical features and genetic variants of three Chinese pedigrees affected with Limb girdle muscular dystrophy type 2I (LGMD2I).METHODS:Clinical data and peripheral blood samples of the three probands and their family members were collected. Whole exome sequencing was carried out for the probands. Candidate variants were verified by Sanger sequencing of their family members.RESULTS:Probands 1 and 2 both featured weakness in the lower limbs. Proband 1 had lost walking ability and had pulmonary ventilation dysfunction. Proband 3 had lower limb pain, palpitations and asthma after exercise. Genetic sequencing revealed that proband 1 harbored compound heterozygous c.545A>G (p.Y182C) and c.1391A>T (p.N464I) variants of the FKRP gene, proband 2 harbored compound heterozygous c.545A>G (p.Y182C) and c.941C>T (p.T314M) variants of the FKRP gene, and proband 3 harbored compound heterozygous c.545A>G (p.Y182C) and c.161G>A (p.R54Q) variants. Among these, the c.161G>A (p.R54Q) variant was unreported previously.CONCLUSION:Compound heterozygous variants of the FKRP gene probably underlay the LGMD2I in the three patients. Whole exome sequencing is crucial for the diagnosis of LGMD2I. The identification of the novel variant also broadened the mutational spectrum of the FKRP gene.

INTRODUCTION:Limb-girdle muscular dystrophy (LGMD) is a group of clinically heterogeneous muscle disorders commonly manifesting proximal limb girdle muscle weakness. There have been more than 30 subtypes of LGMD associated with causative genes and limb-girdle muscular dystrophy type 2J (LGMD2J) is caused by mutations in the TTN gene.METHODS:We report a Han Chinese family with LGMD2J. The proband and his sister both presented with weakness in the proximal lower limbs bilaterally. Muscle biopsy and genetic analysis were performed.RESULTS:Muscle biopsy of the proband showed dystrophic changes accompanied by rimmed vacuoles. Whole-exome sequencing identified novel compound heterozygous mutations in the TTN gene, including elongation (c.107962_107963delAT, p.I35988Sfs*26) and truncation (c.99125_99128dupACAG, p.S33043Rfs*9) variants in the proband and his sister. Both two variants have never been reported. Notably, we are the first to identify an elongation mutation in the TTN gene, broadening the genetic mutation spectrum of LGMD2J.DISCUSSION:Several variants in the last exon of the TTN gene have been reported, one of which was associated with LGMD2J. Besides, LGMD2J should be distinguished from other myopathies caused by mutations in the TTN gene. The pathogenesis of and specific curative methods for LGMD2J remain to be further elucidated.

Limb-girdle muscular dystrophy 2G (LGMD2G) is a subtype of limb-girdle muscular dystrophy. However, the disease's mechanisms are still not fully understood, and no established therapeutic targets have been found. Using a morpholino-based knockdown approach, we established an LGMD2G zebrafish model. In this study, we found that the ROS level increased in LGMD2G zebrafish. The expression of the mitophagy-related protein BNIP3L, LC3A-II/LC3A-I, and LAMP1 were increased in LGMD2G zebrafish. The oxygen consumption rate and citrate synthase expression was significantly decreased. Thus, mitophagy was presumed to be involved in the LGMD2G to reduce ROS levels. Then, we administered vitamin C, coenzyme Q10, idebenone, metformin, or dexamethasone to rescue LGMD2G in zebrafish. Idebenone reduced the curly tail phenotype and ROS level. Also, it reduced BNIP3L expression in LGMD2G zebrafish models and improved their motor function. In conclusion, mitophagy might be involved in the LGMD2G, and idebenone ameliorated LGMD2G by downregulating ROS level.

目的 探讨影响泛耐药鲍曼不动杆菌(Extensively Drug resistance Acinetobacter baumannii,XDRAB)感染预后的危险因素.方法 回顾性收集2011年1月至2016年12月在上海市第六人民医院住院且发生XDRAB感染的患者的临床资料,应用单因素分析及多因素logistic回归分析影响XDRAB感染预后的危险因素.结果 157例XDRAB感染患者中存活90例,死亡67例,死亡率42.68％,logistic多因素回归分析发现,年龄≥65岁、合并心功能不全、住院期间有创通气、住院期间联合抗真菌药物、感染时CRP≥184.63 mg/L、住院期间谷丙转氨酶≥141U/L、住院期间尿素氮≥14.3 mmol/L为影响XDRAB感染预后的独立危险因素,感染XDRAB后抗生素使用持续时间≥6天,是XDRAB感染预后的独立保护因素.结论 XDRAB感染死亡率高,高龄、基础疾病重、CRP明显升高、联用抗真菌药物是预后不良的主要因素,减少并发症发生,避免抗真菌药物滥用,适当延长感染XDRAB后抗生素治疗时间,有利于改善预后.

OBJECTIVES: We compared the diagnostic potential of cancer ratio (CR, serum lactate dehydrogenase [LDH]/pleural fluid adenosine deaminase [pfADA]), cancer ratio plus (CR plus, cancer ratio/pleural lymphocyte percentage), and age/pfADA ratio with pfADA in malignant pleural effusion. METHODS: Data from 100 patients with malignant pleural effusion (MPE) and 119 patients with tuberculous pleural effusion (TPE) were retrospectively collected. PfADA, age/pfADA ratio, CR, and CR plus were compared between patients with MPE and those with TPE in two age groups (≤50 and >50 years). The best cut-off value was determined, and the diagnostic performance was evaluated according to the receiver operating characteristic curve. RESULTS: PfADA was statistically significantly lower while age/pfADA ratio, CR, and CR plus were significantly higher in the MPE group than in the TPE group in both age groups (p<0.05). For patients aged ≤50 years, the differential diagnostic value of pfADA for MPE was better than those of age/pfADA ratio, CR, and CR plus. At a cut-off value of 13.0 U/L, the sensitivity, specificity, and accuracy were 88.9%, 100.0%, and 98.9%, respectively. For patients aged >50 years, the diagnostic performance of CR plus was superior to those of pfADA, age/pfADA ratio, and CR. At a cut-off value of 22.6, the sensitivity, specificity, and accuracy of CR plus for the diagnosis of MPE were 86.8%, 84.6%, and 86.2%, respectively. CONCLUSIONS: The best parameter for diagnosing MPE was different for patients aged ≤50 years and >50 years. For patients aged >50 years, CR plus was a good parameter for the differential diagnosis of MPE. For patients aged ≤50 years, pfADA was better.

Hereditary myopathy with early respiratory failure (HMERF) is a subtype of myofibrillar myopathy. Mutations located on exon 344 of the titin-A band, the 119th fibronectin-3 domain (FN3 119), are responsible for HMERF. In this article, we retrospectively analyzed the clinical features, findings of muscle imaging, muscle pathology, immunohistochemistry, and ultrastructural characteristics of seven patients diagnosed with HMERF at a single center in China. Muscle MRI showed the involvement of semitendinosus in four patients. The common pathological features were variability in fiber diameter, increased internal nuclei, endomysial fibrosis, and cytoplasmic bodies. On immunohistochemical examination, the cytoplasmic bodies stained positive for calpain-3, p53, and programmed death-ligand 1. Electron microscopy showed cytoplasmic bodies, distorted sarcomere architecture, glycogen pool, and subsarcolemmal accumulation of mitochondria and lysosomes. We retrospectively reviewed four reported HMERF patients in China. Among the 11 patients, the median age at onset was 34 years (range 14–54). Allelic frequency of mutation c.95195C > T was 36.36%. This study characterizes the phenotype and genotype spectrum of HMERF in China.

Background: Accumulating evidence has revealed that human gingiva-derived mesenchymal stem cells (GMSCs) are emerging as a new line of mesenchymal stem cells and have a robust immune regulatory function and regenerative ability. However, the relationship between immune regulatory function and regenerative ability is unclear, whether GMSCs promoted osteoblastic differentiation by regulating immune cells. Methods: In this study, we investigated the effect of GMSCs regulating T-cell biological activity on osteoblasts in a direct contact co-culture system. GMSCs and T-cell were co-cultured, the co-culture supernatant was collected and acted on MC3T3-E1 cells, then the alkaline phosphatase (ALP) staining, Alizarin Red staining, Immunofluorescence staining, and real-time quantitative PCR (RT-qPCR) analysis of osteogenic genes were detected to evaluated the osteogenesis differentiation of MC3T3-E1 cells. Results: Our results demonstrated that GMSCs could suppress the activated T-cell function by downregulation pro-inflammatory cytokines (Interleukin-1β [IL-1β] and Tumor necrosis factor-α [TNF-α]) and the upregulation of anti-inflammatory cytokines (IL-10). Meanwhile, the co-culture supernatant significantly increased osteogenic differentiation of ME3T3-E1. Conclusion: GMSCs could promote the osteogenic differentiation of MC3T3-E1 cells by inhibiting the biological activity of activated T-cell.

PURPOSE This study aimed at exploring the effect of berberine (C20H18NO4) on osteogenic differentiation of rat adipose-derived stem cells(ADSCs) and clarifying the related mechanism. METHODS ADSCs were subjected to 5, 10, 20 μmol/L berberine culture solution. The untreated ADSCs were set as the control group. Cell proliferation activity was determined by MTT method. Alkaline phosphatase (ALP) staining, semi-quantitative assay and alizarin red staining (ARS) were applied to analyze the effect of berberine on osteogenic differentiation of ADSCs. The phosphorylation level of c-Jun amino terminal kinase (JNK) protein was tested by Western blot. Runx2, OCN were tested by Western blot before and after application of JNK pathway inhibitor SP600125. SPSS 22.0 software package was used for statistical analysis. RESULTS There was no significant difference on cell proliferation activity of ADSCs treated with 5, 10 and 20 μmol/L berberine at 1, 3 and 7 day(P>0.05). ALP staining and ARS staining in groups treated by berberine were significantly darker than those of the control group, and ALP protein secretion in the experimental group was significantly up-regulated (P<0.05). The phosphorylation level of JNK was increased after treated with 10 μmol/L berberine culture medium. The expression of osteogenic related proteins Runx2 and OCN was up-regulated in the experimental group. After inhibition of JNK signaling pathway, the expression of Runx2 and OCN was down-regulated. CONCLUSIONS Berberine has no effect on cell proliferation of ADSCs, and can up-regulate osteogenic differentiation of ADSCs through activation of JNK signaling pathway.

目的 建立区分呼吸系统泛耐药鲍曼不动杆菌(XDRAB)感染与定植的评分系统.方法 选择2011年1月至2016年12月在上海市第六人民医院呼吸道标本培养出XDRAB的患者272例(定植142例,感染130例).利用单因素分析进行筛选,然后使用多因素logistic回归分析发现感染的独立预测因素并建立评分系统,采用ROC曲线评价该评分系统,并进行准确性验证.结果 通过建模样本建立评分系统:Z=42×培养出XDRAB时最高体温(≥38℃为1分,<38℃为0分)+18×新出现症状或原有症状加重(是为1分,否为0分)+32×白细胞数(≥10.6×109/L为1分,反之为0分)+43×胸部影像学变化(新出现炎性浸润影或炎性浸润影加重为1分,否则为0分),该评分系统ROC曲线下面积为0.973(95％CI:0.954～0.992).当Z<75分时考虑为定植,≥75分时考虑为感染.在测试样本中该评分系统对XDRAB感染和定植的预测与实际相符率为85.56％,阳性预测值为0.930,阴性预测值为0.787.结论 该评分系统能较准确地区分呼吸系统XDRAB的感染和定植,从而为治疗提供依据.

We report a 26-year-old man with left chest pain for 4 days. His chest CT showed a cavity in the left upper lung. Tuberculosis was suspected first, but metagenomics next generation sequencing (mNGS) in bronchoalveolar lavage fluid only detected Tropheryma whipplei. Tropheryma whipplei is the pathogen of Whipple’s disease. The most frequently involved organs are the eyes, heart, and central nervous system. Pulmonary parenchymal involvement is rare. To our knowledge, this is the first reported case of pulmonary cavity caused by Tropheryma whipplei. Nineteen cases of pulmonary parenchymal involvement were found by literature search. The most common respiratory symptom was cough, followed by dyspnea/breathlessness and chest pain. The most common finding in chest imaging was pulmonary nodules, followed by interstitial changes and patchy infiltration. Our case and literature review highlighted that Tropheryma whipplei infection should be considered in the differential diagnosis of pulmonary cavity, pulmonary nodules, interstitial changes, and patchy infiltration. mNGS is helpful to improve diagnosis rate.

Background Tuberculous pleural effusion (TPE) is usually characterized by lymphocytic predominance and high pleural fluid adenosine deaminase (pfADA), while parapneumonic pleural effusion (PPE) is usually characterized by neutrophilic predominance. However, in some cases, neutrophils can be predominant in TPE. In such cases, the differential diagnosis between TPE and PPE is challenging and has been rarely investigated. The aim of this study was to evaluate the accuracy of pfADA, pleural fluid lactate dehydrogenase (pfLDH) and other parameters, such as age/pfADA in the differential diagnosis of neutrophil-predominant TPE (NP-TPE) and PPE. Methods Between January 2003 and August 2018, 19 patients with NP-TPE and 54 patients with PPE at Shanghai Jiao Tong University Affiliated Sixth People's Hospital were retrospectively reviewed. Age, blood and pleural fluid findings, and eight ratios that consisted of routine biomarkers were compared between the two groups in ≤50 and >50 years old groups. ROC curve analysis was used to evaluate diagnostic performance. Results The three parameters with the largest AUC were age/pfADA, pfADA and pfLDH in ≤ 50 years old group, and pfADA, age/pfADA and the percentage of neutrophils in pleural fluid (pfN%) in >50 years old group. For patients ≤ 50 years old, pfADA combined with pfLDH or age/pfADA combined with pfLDH could increase the specificity to 100%, while the sensitivity of the former was high (84.6% vs 76.9%). For patients >50 years old, both pfADA combined with pfN% and age/pfADA combined with pfN% could increase the specificity to 90.3% with the same sensitivity. Conclusions Although pfADA played an important role in the discrimination of NP-TPE from PPE, combining pfADA with pfLDH for patients ≤50 years old or combining pfADA with pfN% for patients >50 years old might improve diagnostic performance.

The guided bone regeneration (GBR) concept has been extensively utilized to treat maxillofacial bone defects in clinical practice. However, the repair efficacy of currently available GBR membranes is often compromised by their limited bone regeneration potential and deficient antibacterial activity. In this study, inspired by the bi-layered structure design of the commonly used Bio-GideⓇmembrane, we designed and fabricated a new kind of multifunctional bi-layered "GBR scaffold" combining solution electrospinning writing (SEW) and solution electrospinning (SES) techniques using a single SEW printer. Copper-loaded mesoporous silica nanoparticles (Cu@MSNs) were incorporated into the poly(lactic-co-glycolic acid)/gelatin (PLGA/Gel, denoted as PG) fiber matrix to construct a composite PG-Cu@MSNs fibrous scaffold. The obtained GBR scaffold consisted of a loose and porous SEW layer to support and facilitate bone ingrowth, and a dense and compact SES layer to resist non-osteoblast interference. The resulting enhanced mechanical properties, coordinated degradation profile, and facile preparation procedure imparted the composite scaffold with good clinical feasibility. In vitro biological experiments indicate that the PG-Cu@MSNs composite scaffold exhibited favorable osteogenic and antibacterial properties. Furthermore, an in vivo rat periodontal defect model further confirmed the promising bone regeneration efficacy of the PG-Cu@MSNs scaffold. In conclusion, the developed electrowritten Cu@MSNs-incorporated bi-layered scaffold with hierarchical architecture and concurrent osteogenic and antibacterial functions may hold great potential for application in GBR.

目的:研究PH797804对脂多糖/D-氨基半乳糖氨(Lipopolysaccharide/D-galactosamine,LPS/D-Gal)诱导的急性肝衰竭(Acute liver failure,ALF)小鼠的保护作用及机制.方法:将64只小鼠随机分成四组,每组16只.腹腔注射LPS/D-Gal诱导建立小鼠ALF模型,设立生理盐水对照组(a)、LPS/D-Gal诱导模型组(b)、LPS/D-Gal诱导和PH797804干预组(c)及PH797804处理对照组(d).观察小鼠48h内的存活率,检测血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)的含量,HE染色组织切片观察肝脏病理变化,Elisa检测血清中TNF-αt和IL-6的表达水平,并对各组小鼠肝组织进行高通量转录组测序以探寻作用机制,采用Real-timePCR法验证测序结果.结果:相比于ALF模型组小鼠,PH797804处理后c组小鼠48 h存活率从20％提高至80％,小鼠肝脏组织病理学异常显著改善,血清中ALT、AST含量较ALF模型组相比显著降低(P＜0.01),血清中TNF-α和IL-6等促炎细胞因子含量较ALF模型组相比显著降低(P＜0.0l).RNA测序结果提示PH797804对LPS/D-Gal诱导小鼠ALF的保护作用主要与抑制炎症反应相关.Real-time PCR验证了测序结果的可靠性.结论:PH797804对LPS/D-Gal诱导的小鼠ALF具有保护作用,其作用机制可能与抑制炎症反应有关.