Body mass index's effect on CRSwNP extends to pathological endotype and recurrence.

BACKGROUND: Elevated body mass index (BMI) has been recognized as an important contributor to corticosteroid insensitivity in chronic rhinosinusitis with nasal polyps (CRSwNP). We aimed to delineate the effects of elevated BMI on immunological endotype and recurrence in CRSwNP individuals. METHODOLOGY: A total of 325 patients with CRSwNP undergoing FESS were recruited and stratified by BMI. H&E staining was employed for histological evaluation. Characteristics of inflammatory patterns were identified by immunohistochemical staining. The predictive factors for recurrence were determined and evaluated by multivariable logistic regression analysis and the receiver operating characteristic (ROC) curves across all subjects and by weight group. RESULTS: In all patients with CRSwNP, 26.15% subjects were classified as overweight/obese group across BMI categories and exhibited a higher symptom burden. The upregulated eosinophil/neutrophil-dominant cellular endotype and amplified type 2/ type 3 coexisting inflammation was present in overweight/obese compared to underweight/normal weight controls. Additionally, a higher recurrent proportion was shown in overweight/obese patients than that in underweight/normal weight cohorts. Multivariable logistic regression analysis identified BMI as an independent predictor for recurrence. The predictive capacity of each conventional parameter (tissue eosinophil and CLCs count, and blood eosinophil percentage) alone or in combination was poor in overweight/obese subjects. CONCLUSIONS: Overweight/obese CRSwNP stands for a unique phenotype and endotype. Conventional parameters predicting recurrence are compromised in overweight/obese CRSwNP, and there is an urgent need for novel biomarkers that predict recurrence for these patients.

High Lithium Storage Performance of Co Ion-Doped Li4Ti5O12 Induced by Fast Charge Transport.

In this study, Co3O4-doped Li4Ti5O12 (LTO) composite was designed and synthesized by the hydrothermal reduction method and metal doping modification method. The microstructure and electrochemical performance of the Co3O4-doped Li4Ti5O12 composite were characterized by XRD, SEM, TEM, electrochemical impedance spectroscopy, and galvanostatic tests. The results showed that Li4Ti5O12 particles attached to lamellar Co3O4 constituted a heterostructure and Co ion doped into Li4Ti5O12 lattice. This Co ion-doped microstructure improved the charge transportability of Li4Ti5O12 and inhibited the gas evolution behavior of Li4Ti5O12, which enhanced the lithium storage performance. After 20 cycles, the discharge specific capacity reached stability, and the capacity retention maintained 99% after 1,000 cycles at 0.1 A/g (compared to the capacity at the 20th cycle). It had an excellent rate performance and long cycle stability, in which the capacity reached 174.6 mA h/g, 2.2 times higher than that of Li4Ti5O12 at 5 A/g.

Design of Ni(OH)2/M-MMT Nanocomposite With Higher Charge Transport as a High Capacity Supercapacitor.

Nano-petal nickel hydroxide was prepared on multilayered modified montmorillonite (M-MMT) using one-step hydrothermal method for the first time. This nano-petal multilayered nanostructure dominated the ion diffusion path to be shorted and the higher charge transport ability, which caused the higher specific capacitance. The results showed that in the three-electrode system, the specific capacitance of the nanocomposite with 4% M-MMT reached 1068 F/g at 1 A/g and the capacity retention rate was 70.2% after 1,000 cycles at 10 A/g, which was much higher than that of pure Ni(OH)2 (824 F/g at 1 A/g), indicating that the Ni(OH)2/M-MMT nanocomposite would be a new type of environmentally friendly energy storage supercapacitor.

[Clinical, pathological and genetic characteristics of 8 patients with distal hereditary motor neuropathy].

OBJECTIVE: Distal hereditary motor neuropathy (dHMN) comprises a heterogeneous group of inherited disorders associated with neurodegeneration of motor nerves and neurons, mainly charac-terized by progressive atrophy and weakness of distal muscle without clinical or electrophysiological sensory abnormalities. To improve the recognition and diagnosis of the disease, we summarized the clinical manifestations, electrophysiological, pathological, and genetic characteristics in eight patients with dHMN. METHODS: Eight probands from different families diagnosed with dHMN were recruited in this study between June 2018 and April 2019 at Peking University People's Hospital. Eight patients underwent complete neurological examination and standard electrophysiological examinations. The clinical criteria were consistent with the patients presenting with a pure motor neuropathy with no sensory changes on electrophysiology. The detailed clinical symptoms, neurophysiological examinations, pathological features and gene mutations were analyzed retrospectively. Genetic testing was performed on the eight patients using targeted next-generation sequencing panel for inherited neuromuscular disorder and was combined with segregation analysis. RESULTS: The age of onset ranged between 11 and 64 years (median 39.5 years) in our dHMN patients. All the cases showed a slowly progressive disease course, mainly characterized by distal limb muscle weakness and atrophy. The motor nerve conduction revealed decreased compound muscle action potential amplitude and velocity, while the sensory nerve conduction velocities and action potentials were not affected. Needle electromyography indicated neurogenic chronic denervation in all patients. Muscle biopsy performed in two patients demonstrated neurogenic skeletal muscle damage. Sural nerve biopsy was performed in one patient, Semithin sections shows relatively normal density and structure of large myelinated fibers, except very few fibers with thin myelin sheaths, which suggested very mild sensory nerve involvement. Eight different genes known to be associated with dHMN were identified in the patients by next-generation sequencing, pathogenic dHMN mutations were identified in three genes, and the detection rate of confirmed genetic diagnosis of dHMN was 37.5% (3/8). Whereas five variants of uncertain significance (VUS) were identified, among which two novel variants co-segregated the phenotype. CONCLUSION: dHMN is a group of inherited peripheral neuropathies with great clinical and genetic heterogeneity. Next-generation sequencing is widely used to discover pathogenic genes in patients with dHMN, but more than half of the patients still remain genetically unknown.

Activation of central galanin receptor 2 mitigated insulin resistance in adipocytes of diabetic rats.

PURPOSE: Our and other's studies showed that administration of neuropeptide galanin may mitigate insulin resistance via promoting glucose transporter 4 (GLUT4) expression and translocation in rats. The objective of this study is to investigate whether galanin receptor 2 (GAL2-R) in brain mediates the ameliorative effect of galanin on insulin resistance in adipose tissues of type 2 diabetic rats. METHODS: In this study galanin, GAL2-R agonist M1145 and GAL2-R antagonist M871 were respectively or cooperatively injected into intracerebroventricles of type 2 diabetic rats once a day for successive fifteen days. Then the plasma and fat tissues of rats were used to estimate the alterations of insulin resistance indexes. RESULTS: The central administration of galanin enhanced 2-deoxy-[3H]-D-glucose, peroxisome proliferator-activated receptor γ and adiponectin levels, food intake and body weight, GLUT4 mRNA expression and GLUT4 concentration in plasma membranes, as well as homeostasis model assessment-insulin resistance index. Those effects of galanin may be blocked by M817, and imitated by M1145 except for food intake and body weight. CONCLUSION: Those results suggest that central GAL2-R mediates the beneficial effects of galanin on insulin sensitivity in type 2 diabetic rats. GAL2-R agonist may be taken as a potential antidiabetic agent to treat insulin resistance and type 2 diabetes.

The Microbiome as a Modifier of Neurodegenerative Disease Risk.

The gut microbiome is increasingly implicated in modifying susceptibility to and progression of neurodegenerative diseases (NDs). In this review, we discuss roles for the microbiome in aging and in NDs. In particular, we summarize findings from human studies on microbiome alterations in Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease. We assess animal studies of genetic and environmental models for NDs that investigate how manipulations of the microbiome causally impact the development of behavioral and neuropathological endophenotypes of disease. We additionally evaluate the likely immunological, neuronal, and metabolic mechanisms for how the gut microbiota may modulate risk for NDs. Finally, we speculate on cross-cutting features for microbial influences across multiple NDs and consider the potential for microbiome-targeted interventions for NDs.

Proteasomal degradation of the intrinsically disordered protein tau at single-residue resolution.

Intrinsically disordered proteins (IDPs) can be degraded in a ubiquitin-independent process by the 20S proteasome. Decline in 20S activity characterizes neurodegenerative diseases. Here, we examine 20S degradation of IDP tau, a protein that aggregates into insoluble deposits in Alzheimer's disease. We show that cleavage of tau by the 20S proteasome is most efficient within the aggregation-prone repeat region of tau and generates both short, aggregation-deficient peptides and two long fragments containing residues 1 to 251 and 1 to 218. Phosphorylation of tau by the non-proline-directed Ca2+/calmodulin-dependent protein kinase II inhibits degradation by the 20S proteasome. Phosphorylation of tau by GSK3ß, a major proline-directed tau kinase, modulates tau degradation kinetics in a residue-specific manner. The study provides detailed insights into the degradation products of tau generated by the 20S proteasome, the residue specificity of degradation, single-residue degradation kinetics, and their regulation by posttranslational modification.

Long non-coding RNA DANCR induces chondrogenesis by regulating the miR-1275/MMP-13 axis in synovial fluid-derived mesenchymal stem cells.

OBJECTIVE: The aim of this study was to examine the role of lncRNA-differentiation antagonizing non-protein coding RNA (DANCR) and its underlying mechanisms in chondrogenesis, more specifically in synovial fluid-derived mesenchymal stem cell (SFMSCs). MATERIALS AND METHODS: The expression levels of DANCR in SFMSCs were measured by qRT-PCR. Luciferase reporter assay and RIP assay were used to investigate the direct target of DANCR and miR-1275 in SFMSCs. The expression of matrix metallopeptidase 13 (MMP13, also known as chondrogenic marker) protein was examined by Western blot. Cell proliferation was analyzed by Cell Counting Kit-8 (CCK-8) assay, while chondrogenic differentiation was explored by sGAG assay. RESULTS: Our data indicated that DANCR can promote SFMSCs proliferation and chondrogenesis. In addition, miR-1275 was indicated as a direct target of DANCR. MiR-1275 was negatively regulated by DANCR via competing endogenous RNA (ceRNA) mechanism. Moreover, our data revealed that miR-1275 could bind to MMP13 and regulate its expression. CONCLUSIONS: Our findings suggested that DANCR was involved in SFMSCs proliferation and chondrogenesis. Mechanistically, DANCR functions as a sponge RNA for miR-1275 that regulates the expression of target gene MMP13. These data provide a therapeutic option for Osteoarthritis (OA).

Cooperation between galanin and insulin in facilitating glucose transporter 4 translocation in adipose cells of diabetic rats.

The glucose transporter 4 (GLUT4) translocation is a vital link of insulin-induced glucose uptake in adipose tissue and skeletal muscle. It is an important topic in anti-diabetic research to explore novel agents to facilitate the role of insulin. The aim of this study was to verify the hypothesis that neuropeptide galanin may enhance insulin-induced GLUT4 translocation to increase glucose uptake in adipose tissue of type 2 diabetic models. Insulin and/or galanin were injected respectively or cooperatively into type 2 diabetic rats once a day for fifteen days. The results showed that administration of galanin significantly enhanced insulin-induced GLUT4 and vesicle-associated membrane protein 2 (VAMP2) translocation, Akt phosphorylation and glucose uptake, but not GLUT4 mRNA and protein expression levels in adipose cells. The beneficial roles of galanin on insulin-induced events may be blocked by MK-2206, an Akt inhibitor, indicating that the Akt phosphorylation is essential for promoting impact of galanin on the insulin-induced events. These results suggest that galanin may benefit insulin-induced GLUT4 and VAMP2 translocation, and subsequent glucose uptake via the activated Akt-VAMP2-GLUT4 pathway in adipose cells. These findings deepen our understanding of the anti-diabetic effect of galanin and its mechanism.

[Review of sixty years of burn discipline in Shanghai Ruijin Hospital].

Department of Burns and Plastic Surgery of Ruijin Hospital Affiliated to the Medical School of Shanghai Jiao Tong University is derived from the group of severe burn treatment in Surgical Department of Kuang-Ci Hospital in Shanghai in 1958. In three score years, they created and developed distinctive technologies in treatment of massive deep burns, including early eschar excision on deep burn wound by stages and batches, taking the scalp as a donor site, wound covering with the large sheet of allo- or xeno-skin graft with small holes covered by small pieces of autoskin, the Ruijin formula for fluid resuscitation in early stage post burn and the " hibernation remedy" , which achieved actual effects in clinic, and they summed up academically the experiences of their clinical practice and researches. These technologies with other creations by Chinese burn surgeons have been named as " Chinese method" of burn treatment.

Correlations of complication with coronary arterial lesion with VEGF, PLT, D-dimer and inflammatory factor in child patients with Kawasaki disease.

OBJECTIVE: To investigate the correlations of complication with coronary arterial lesion (CAL) or not with vascular endothelial growth factor (VEGF), platelet (PLT), D-dimer, and inflammatory factor in child patients with Kawasaki disease (KD). PATIENTS AND METHODS: A total of 60 KD child patients meeting the inclusion criteria diagnosed and treated from January 2016 to October 2017 were collected. There were 27 child patients complicated with CAL enrolled as observation group and 33 child patients not complicated with CAL selected as control group. The venous blood of the two groups of patients was acquired after admission to hospital. Enzyme-linked immunosorbent assay (ELISA) was utilized to detect the content of serum VEGF and interleukin-6 (IL-6); the content of serum PLT and D-dimer was measured using a fully automatic biochemistry analyzer, and the coronary artery diameter was determined through color Doppler ultrasound. RESULTS: Compared with those in control group, the content of VEGF, IL-6, PLT, and D-dimer in the serum was increased remarkably in the observation group, and the differences were statistically significant (p<0.05). The thickness of the coronary artery in the observation group was markedly greater than that in the control group, with a statistically significant difference (p<0.05). The content of VEGF, IL-6, PLT, and D-dimer in the serum was positively correlated with the thickness of the coronary artery. CONCLUSIONS: For KD child patients, the complication with CAL or not has a close correlation with VEGF, PLT, D-dimer, and inflammatory factor; and VEGF, IL-6, PLT, and D-dimer are the important risk factors for KD complicated with CAL.

[Endoscopic transnasal approach for surgical treatment of skull base clival area chordomas (Report of 2 cases)].

The case 1 performanced submandibular trauma because of the faint Suddenly. There were no obvious abnormality in physical examination. CT result showed that the tumour located in the lower clivus, and the atlas was infringed. MRI imaging showed the tumour located in the both sides of the internal carotid artery, infringed clivus and atlas front, forwarded into the nasal cavity and oral cavity. The case 2 performanced the left nose stuffy and increased gradually, nasopharyngeal mirror showed the left nasal cavity filled with new life. CT showed the lesions located in the cranial fossa under the sella turcica and sphenoid bone, down into the sphenoid sinus and the nasopharyngeal cavity. MRI imaging showed the lesions located in the front of clivus. According to the CT and MRI imaging features before surgery, the two cases adopted endoscopic transsphenoidal approach, and the postoperative pathology were chordoma in the central line of the skull base.

[Ophthalmological health care of the institutionalized elderly : The OVIS study]. / Ophthalmologische Versorgung in Seniorenheimen : Die OVIS-Studie.

BACKGROUND: Due to demographic change and societal transformation the number of elderly persons living in retirement homes is growing in Germany. Access to health care is more complicated in the setting of nursing homes. Different regional studies suggest unmet ophthalmological health care needs in institutionalized elderly people. This study assessed the current ophthalmological health care structure and supply status in nursing homes in Germany. METHODS: This prospective, multicenter cross-sectional study was conducted by 14 study centers in Germany. Elderly people living in 32 nursing homes were included after approval by the local institutional review boards. A standardized examination was performed which included a detailed medical and ocular history, refraction, visual acuity testing, tonometry, biomicroscopy and dilated funduscopy. Unmet ophthalmological health care needs were documented and the data were analyzed descriptively and via logistic regression modelling. RESULTS: A total of 600 participants (434 women and 166 men) aged 50-104 years were examined of which 368 (61%) had ophthalmological conditions requiring treatment. The most prevalent findings were cataracts (315; 53%), disorders of the eyelids (127; 21%), dry eye disease (57; 10%) and posterior capsule opacification (43; 7%). In 63 (11%) of the participants glaucoma was suspected and 55 (9%) of the examined population had a known diagnosis of glaucoma, of whom one third was not on any or on insufficient anti-glaucomatous therapy. 236 (39%) showed signs of age-related macular degeneration (AMD). Only 52% of the examined cohort had been examined by an ophthalmologist within the last 5 years and 39% stated that they would currently not be able to consult an ophthalmologist. Reported barriers were mainly transport and lack of support. CONCLUSION: This study demonstrates considerable unmet ophthalmological health care needs of the institutionalized elderly in Germany. Novel and reformed models of specialist care provision have to be developed.

Therapeutic efficacy of atypical antipsychotic drugs by targeting multiple stress-related metabolic pathways.

Schizophrenia (SZ) is considered to be a multifactorial brain disorder with defects involving many biochemical pathways. Patients with SZ show variable responses to current pharmacological treatments of SZ because of the heterogeneity of this disorder. Stress has a significant role in the pathophysiological pathways and therapeutic responses of SZ. Atypical antipsychotic drugs (AAPDs) can modulate the stress response of the hypothalamic-pituitary-adrenal (HPA) axis and exert therapeutic effects on stress by targeting the prefrontal cortex (PFC) and hippocampus. To evaluate the effects of AAPDs (such as clozapine, risperidone and aripiprazole) on stress, we compared neurochemical profile variations in the PFC and hippocampus between rat models of chronic unpredictable mild stress (CUMS) for HPA axis activation and of long-term dexamethasone exposure (LTDE) for HPA axis inhibition, using an ultraperformance liquid chromatography-mass spectrometry (UPLC-MS/MS)-based metabolomic approach and a multicriteria assessment. We identified a number of stress-induced biomarkers comprising creatine, choline, inosine, hypoxanthine, uric acid, allantoic acid, lysophosphatidylcholines (LysoPCs), phosphatidylethanolamines (PEs), corticosterone and progesterone. Specifically, pathway enrichment and correlation analyses suggested that stress induces oxidative damage by disturbing the creatine-phosphocreatine circuit and purine pathway, leading to excessive membrane breakdown. Moreover, our data suggested that the AAPDs tested partially restore stress-induced deficits by increasing the levels of creatine, progesterone and PEs. Thus, the present findings provide a theoretical basis for the hypothesis that a combined therapy using adenosine triphosphate fuel, antioxidants and omega-3 fatty acids as supplements may have synergistic effects on the therapeutic outcome following AAPD treatment.

Role of Th1/Th2 cytokines in the diagnosis and prognostic evaluation of ankylosing spondylitis.

Ankylosing spondylitis (AS), a progressive disease of the spine, manifests as peripheral arthritis with tendon and ligament inflammation that restricts activity. AS is a rheumatoid autoimmune disease although the rheumatoid factor is absent in patients with AS. It is characterized by inflammatory changes such as elevated levels of serum inflammatory factors. The roles of Th1 and Th2 cytokines in autoimmune diseases are well known. However, the roles of these cytokines in the diagnosis and prognosis of AS is poorly understood. The aim of this study was to investigate the roles of Th1/Th2 cytokines in the diagnosis and prognosis of AS. The BASDAI activity, BASFI functional index, BASMI measurement score, and the levels of CRP and ESR were measured during the treatment of patients with active AS. The levels of IFN-γ and TNF-α (Th1 cytokines) and IL-4 and IL-10 (Th2 cytokines) were quantified. The levels of IL-4 and IL-10 were significantly low in the serum of patients with active AS, who also had high IFN-γ and TNF-α levels compared to those in the control individuals (P < 0.05). After treatment, the levels of IL-4 and IL-10 increased while those of IFN-γ and TNF-α decreased compared to those in individuals with active AS (P < 0.05). The disease activity index correlated positively with levels of IFN-γ and TNF-α and negatively with levels of IL-4 and IL-10, but not with that of CRP or ESR. Changes in the levels of Th1/2 cytokines in patients with AS may reflect disease activity and prognosis.

[Optical coherence tomography angiography (OCT­A) in rats]. / Optische-Kohärenztomographie-Angiographie (OCT­A) bei Ratten.

PURPOSE: Optical coherence tomography angiography (OCT­A) allows for the non-invasive, three-dimensional visualization of retinal and chorioidal vascular structures. In this study, this new imaging modality was evaluated in rats. METHODS: In vivo imaging in Dark Agouti rats was performed using confocal scanning laser ophthalmoscopy (cSLO) and OCT­A (Spectralis prototype, Heidelberg Engineering) after adjusting the length of the reference arm. The OCT­A en-face images were compared to conventional fluorescein angiography cSLO images. The histological examination allowed for correlation of retinal and chorioidal plexus. RESULTS: While the diagnostic device was developed for use in humans, OCT­A and cSLO imaging can be applied in rodents after only minor hardware modifications. High-resolution and contrast-enhanced images enable a depth-selective visualization of the three retinal plexus and the inner and outer chorioidal vascular networks. In comparison to fluorescein angiography (FA), OCT­A is characterized by higher resolution and more accurate three-dimensional localization of vascular structures, particularly in deep layers. A current limitation includes the relatively small area imaged by OCT­A. DISCUSSION: The recently developed OCT­A imaging technology also allows for three-dimensional detection of retinal and chorioidal vascular changes in vivo without dye injection in rodents. OCT may potentially replace invasive FA for specific questions and will be useful in animal models for research of retinal and chorioidal angiogenic processes physiologically and during pharmacological interventions.

Low levels of plasma galanin in obese subjects with hypertension.

BACKGROUND: Obesity is strongly linked to increased blood pressure, which increases the risk of cardiovascular diseases. To our knowledge, little literature reported the information about galanin levels in obese individuals with hypertension. Therefore, the aim of this study was to investigate the possible involvement of galanin in the pathogenesis of obese subjects with hypertension. METHODS: We measured body mass index and blood pressure of 38 obese patients with hypertension, 44 obese controls with normal blood pressure and 44 lean controls with normal blood pressure. Blood samples from all cases were collected at 8:00 a.m. after an overnight fast to determine the fasting plasma concentration of galanin, glucose, insulin, triglyceride, total cholesterol, high- and low-density lipoprotein cholesterol. RESULTS: We found that plasma galanin levels were significantly decreased in obese patients with hypertension compared with the obese control group, whereas the galanin levels were significantly increased in obese controls compared with lean controls. Furthermore, in both obese groups the galanin levels were negatively correlative to diastolic blood pressure and positively correlative to insulin and triglyceride levels, but not to heart rate. CONCLUSIONS: Low galanin levels were one of characters of obese patients with high blood pressure, and this levels may be taken as a novel biomarker to predict the development of high blood pressure in obese patients.

[Effects of ammonium pyrrolidine dithiocarbamate (PDTC) on osteopontin expression and autophagy in tubular cells in streptozotocin-induced diabetic nephropathy rat].

Objective: To investigate the effects of ammonium pyrrolidine dithiocarbamate (PDTC) on tubulointerstitial inflammatory molecules and autophagy in diabetic nephropathy (DN) rats. Methods: Twenty-four male Sprague-Dawley rats were assigned to DN group (n=6) and DN+ PDTC group (n=6, PDTC, ip, 100 mg·kg-1·d-1), all received streptozotocin (STZ) 60 mg/kg intraperitoneally, and the other 12 rats were randomly divided into control group (n=6) and PDTC group (n=6). At the end of 12 weeks, after serum creatine (Scr) and 24-hour urinary protein were determined, rats were sacrificed to determined the renal pathological damages and the changes of nuclear factor (NF)-κB p65, p62, osteopontin (OPN), microtubule associated protein 1 light chain 3 (LC3)-Ⅱ/LC3-Ⅰ, nuclear p-NF-κB p65 by immunohistological stainning and Western blot, and ultrastructural changes of autophagic process was observed by electron microscopy (EM). Results: Scr was similar among the four groups (P>0.05). The levels of urinary protein in DN group and DN + PDTC group were significantly higher than the other two groups (all P<0.01), but the level of urinary protein in DN + PDTC group was lower than that of DN group (P<0.05). DN + PDTC group had less tubulointerstitial damage compared with DN group (P<0.05). Among the four groups, expressions of p62, p65, OPN of tubulointerstitial area in DN group were significantly higher than that of the other groups (all P<0.05), and Western blot showed that DN+ PDTC group had less expressions of NF-κB p65, nuclear p-p65, OPN and more expresssion of LC3-Ⅱ/LC3-Ⅰ compared with DN group (all P<0.05), which were consistent with the decreased autophagic vacuoles and increased mitochondria dysfunction revealed by EM. Correlation analysis showed that renal LC3-Ⅱ/LC3-Ⅰ was negatively correlated the expressions of nuclear p-p65 and OPN (r=-0.45, P=0.02; r=-0.50, P=0.01), and p62 was positively correlated the expressions of nuclear p-p65 and OPN (r=0.33, P=0.01; r=0.41, P=0.01). Conclusion: Tubular NF-κB activation is closely related to autophagy dysfunction in DN rats, and PDTC may enhance autophagy activity in tubule cells by blocking NF-κB activity.