Platycodin D regulates high glucose-induced ferroptosis of HK-2 cells through glutathione peroxidase 4 (GPX4).

Diabetic nephropathy (DN) is associated with inflammation. Platycodin D (PD) demonstrates anti-inflammatory activity. However, whether PD affects DN remains to be explored. Here, we aimed to discuss the role of PD in DN and its underlying mechanisms. High glucose (HG)-induced HK-2 cells were treated with PD, and cell viability was assessed using the Thiazolyl Blue Tetrazolium Bromide (MTT) assay. Ferroptosis-related factors such as lactate dehydrogenase (LDH) activity, lipid reactive oxygen species (ROS), iron (Fe2+) level, GSH level, and malondialdehyde (MDA) level were evaluated. Cell death was evaluated using the TUNEL assay. GPX4 expression was evaluated using Quantitative Real-time PCR (qRT-PCR) and Western blotting analysis. The results indicated that HG increased LDH activity, lipid ROS production, Fe2+ levels, and MDA levels and decreased GSH levels, suggesting that the HG condition induced ferroptosis. PD treatment inhibited ferroptosis in HG-induced cells, downregulated ACSL4 and TFR1 expression, and upregulated FTH-1 and SLC7A11 expression. PD reversed the effects of HG condition on cell death. Moreover, GPX4 expression was downregulated in HG-stimulated cells. Furthermore, we substantiated that PD suppressed ferroptosis by modulating GPX4 expression. In conclusion, PD inhibited ferroptosis in HG-induced HK-2 cells by upregulating GPX4 expression, suggesting that PD may be an effective drug for the clinical treatment of DN.

Cerebral arterial fenestration associated with stroke and other cerebrovascular diseases.

BACKGROUND: Cerebral arterial fenestration is a rare vascular malformation that has not been fully understood. Whether it is related to cerebrovascular diseases remains to be determined. In this study, we aimed to investigate the imaging characteristics of cerebral fenestrations, the clinical characteristics of fenestrations complicated with cerebrovascular diseases, and the correlation between fenestrations and cerebrovascular diseases. METHODS: We reviewed the magnetic resonance imaging and computed tomography (CT) imaging findings of patients with cerebrovascular fenestrations in the Third Affiliated Hospital of Soochow University from January 2016 to December 2020, mainly focused on the shape and location of fenestrations. According to the location of fenestrated arteries, patients were divided into the internal carotid arterial system (ICAS) group and the vertebrobasilar arterial system (VAS) group. For patients complicated with cerebrovascular diseases, detailed data about the demographics and clinical characteristics were recorded. Stroke patients with injured lesions located in the territories of fenestrated arteries were further screened out and analyzed. Moreover, the proportions of cerebrovascular diseases including stroke between the ICAS group and the VAS group were compared. RESULTS: A total of 280 cerebrovascular fenestrations were found in 274 patients (six patients had two fenestrations). The most frequently involved vessels were the anterior cerebral artery (123/280), the basilar artery (76/280) and the vertebral artery (35/280). As to the shape of fenestrations, slit-like fenestrations accounted for 63.2% (177/280), followed by convex-lens-like type 26.1% (73/280) and duplicated type 10.7% (30/280). A total of 70 patients were complicated with cerebrovascular diseases, including ischemic stroke 64.3% (45/70), hemorrhagic stroke 22.9% (16/70), aneurysm 10% (7/70), arteriovenous malformation 1.4% (1/70) and cavernous hemangioma 1.4% (1/70). There were no significant differences between the ICAS group and the VAS group in terms of the demographics and clinical characteristics. Furthermore, among the 61 patients complicated with stroke, 16 patients' stroke lesions were located in the territories of fenestrated arteries, including 12.5% (2/16) in the ICAS and 87.5% (14/16) in the VAS. In addition, compared with the ICAS group, the proportions of cerebrovascular diseases including stroke in patients with fenestrations were higher in the VAS group (P < 0.05). CONCLUSIONS: Cerebral arterial fenestrations are most commonly found in the anterior cerebral artery, the basilar artery and the vertebral artery. Vertebrobasilar fenestrations are more related to cerebrovascular diseases, especially stroke.

Long non-coding RNA PSMA3-AS1 promotes glioma progression through modulating the miR-411-3p/HOXA10 pathway.

BACKGROUND: Glioma is a common type of brain tumor and is classified as low and high grades according to morphology and molecules. Growing evidence has proved that long non-coding RNAs (lncRNAs) play pivotal roles in numerous tumors or diseases including glioma. Proteasome 20S subunit alpha 3 antisense RNA 1 (PSMA3-AS1), as a member of lncRNAs, has been disclosed to play a tumor-promoting role in cancer progression. However, the role of PSMA3-AS1 in glioma remains unknown. Therefore, we concentrated on researching the regulatory mechanism of PSMA3-AS1 in glioma. METHODS: PSMA3-AS1 expression was detected using RT-qPCR. Functional assays were performed to measure the effects of PSMA3-AS1 on glioma progression. After that, ENCORI ( http://starbase.sysu.edu.cn/ ) database was used to predict potential genes that could bind to PSMA3-AS1, and miR-411-3p was chosen for further studies. The interaction among PSMA3-AS1, miR-411-3p and homeobox A10 (HOXA10) were confirmed through mechanism assays. RESULTS: PSMA3-AS1 was verified to be up-regulated in glioma cells and promote glioma progression. Furthermore, PSMA3-AS1 could act as a competitive endogenous RNA (ceRNA) for miR-411-3p to regulate HOXA10 and thus affecting glioma progression. CONCLUSION: PSMA3-AS1 stimulated glioma progression via the miR-411-3p/HOXA10 pathway, which might offer a novel insight for the therapy and treatment of glioma.

Efficacy of pramipexole combined with levodopa for Parkinson's disease treatment and their effects on QOL and serum TNF-α levels.

PURPOSE: To investigate the efficacy of combining the dopamine receptor agonist pramipexole with levodopa for Parkinson's disease (PD) treatment and to measure their effects on quality of life and tumor necrosis factor (TNF)-α levels in PD patients. BASIC PROCEDURE: In total, 160 PD patients who were admitted to our hospital were equally randomized into a control treatment group (levodopa alone) and the study group (pramipexole combined with levodopa). Both groups were treated for 12 weeks. FINDINGS: After treatment, scores from the Unified Parkinson's Disease Rating Scales (1-3), the Hamilton Depression Scale, and the Parkinson's Disease Questionnaire (PDQ-39) were significantly decreased in both groups, whereas Mini-Mental State Examination scores were significantly increased. After treatment, the study group had significantly lower scores for all scales except the Mini-Mental State Examination, for which those who received combined treatment had significantly higher scores than the control group. The incidence of adverse reactions was significantly lower in the study group than in the control group. Furthermore, after treatment, serum TNF-α levels were significantly decreased in both groups compared with pre-treatment levels. CONCLUSION: Pramipexole combined with levodopa relieved PD symptoms and improved the quality of life of PD patients, potentially by suppressing serum TNF-α levels.

The delta-opioid receptor and Parkinson's disease.

Parkinson's disease (PD) is a common degenerative neurological disease leading to a series of familial, medical, and social problems. Although it is known that the major characteristics of PD pathophysiology are the dysfunction of basal ganglia due to injury/loss of dopaminergic neurons in the substantia nigra pars compacta dopaminergic and exhaustion of corpus striatum dopamine, therapeutic modalities for PD are limited in clinical settings up to date. It is of utmost importance to better understand PD pathophysiology and explore new solutions for this serious neurodegenerative disorder. Our recent work and those of others suggest that the delta-opioid receptor (DOR) is neuroprotective and serves an antiparkinsonism role in the brain. This review summarizes recent progress in this field and explores potential mechanisms for DOR-mediated antiparkinsonism.

Effects and mechanism of amyloid ß1-42 on mitochondria in astrocytes.

Amyloid ß (Aß)1-42 is strongly associated with Alzheimer's disease (AD). The effects of Aß1­42 on astrocytes remain largely unknown. The present study focused on the effects of Aß1­42 on U87 human glioblastoma cells as astrocytes for in vitro investigation and mouse brains for in vivo investigation. The mechanism and regulation of mitochondria and cytochrome P450 reductase (CPR) were also investigated. As determined by MTT assays, low doses of Aß1­42 (<1 µM) marginally promoted astrocytosis compared with the 0 µM group within 24 h, however, after 48 h treatment these doses reduced cellular growth compared with the 0 µM group. Furthermore, Aß1­42 doses >5 µM inhibited the growth of U87 cells compared with the 0 µM group after 24 and 48 h treatment. Immunofluorescence analysis demonstrated that astrocytosis was also observed in early stage AD mice compared with wild­type (WT) mice. In addition, concentrations of Aß1­42 were also significantly higher in early stage AD mice compared with WT mice, however, the levels were markedly lower compared with later stage AD mice, as determined by ELISA. In addition to increased levels of Aß1­42 in mice with later stage AD, reduced astrocyte staining was observed compared with WT mice. Western blotting indicated that the effect of Aß1­42 on U87 cell apoptosis may be regulated via Bcl­2 and caspase­3 located in mitochondria, whose functions, including adenosine triphosphate generation, electron transport chain and mitochondrial membrane potential, were inhibited by Aß1­42. During this process, the expression and activity of cytochrome P450 reductase was also downregulated. The current study provides novel insight into the effects of Aß1­42 on astrocytes and highlights a potential role for astrocytes in the protection against AD.

cAMP/PKA signaling pathway contributes to neuronal apoptosis via regulating IDE expression in a mixed model of type 2 diabetes and Alzheimer's disease.

Type 2 diabetes (T2D) may play a relevant role in the development of Alzheimer's disease (AD), however, the underlying mechanism was not clear yet. We developed an animal model presenting both AD and T2D, morris water maze (MWM) test and recognition task were performed to trace the cognitive function. Fasting plasma glucose (FPG) and oral glucose tolerance test (OGTT) were determined to trace the metabolism evolution. TUNEL assay and apoptosis-related protein levels were analyzed for the detection of neuronal apoptosis. Cyclic adenosine monophosphate (cAMP) agonist bucladesine or protein kinase (PKA) inhibitor H-89 were used to determine the effects of cAMP/PKA signaling pathway on IDE expression and neuronal apoptosis. The results showed that T2D contributes to the AD progress by accelerating and worsening spatial memory and recognition dysfunctions. Metabolic parameters and glucose tolerance were significantly changed in the presence of the AD and T2D. The significantly induced neuronal apoptosis and increased pro-apoptotic proteins in mice with AD and T2D were also observed. We showed the decreased expression level of IDE and the activating of cAMP/PKA signaling pathway in AD and T2D mice. Further studies indicated that cAMP agonist decreased the expression level of IDE and induced the neuronal apoptosis in mice with AD and T2D; whereas PKA inhibitor H-89 treatment showed the completely opposite results. Our study indicated that, in the T2D and AD mice, cAMP/PKA signaling pathway and IDE may participate in the contribute role of T2D in accelerating the pathological process of AD via causing the accumulation of Aß and neuronal apoptosis.

In vivo and in vitro studies on the roles of p38 mitogen-activated protein kinase and NADPH-cytochrome P450 reductase in Alzheimer's disease.

Alzheimer's disease (AD) is a chronic neurodegenerative disease with an increasing morbidity rate. As one of the most important signaling pathways that responds to inflammation and degeneration, the p38 mitogen-activated protein kinase (MAPK) signaling pathway is active in the cortexes of AD mice. At the cellular level the same effect can be observed with p38 MAPK when induced by amyloid ß (Aß)1-42, a 42-residue Aß fragment. Inhibition of p38 MAPK in the present study protected SH-SY5Y cells from the toxicity of Aß1-42, and alleviated the formation of senile plaques and cognitive impairment in AD mice. The expression of cytochrome P450 reductase (CPR) in the brains of mice with AD, in addition to Aß1-42-treated SH-SY5Y cells, also increased. However, the inhibition of CPR did not protect SH-SY5Y cells from the toxicity of Aß1-42. The results of the present study suggest that p38 MAPK is a potential therapeutic target for the treatment of AD. In addition, the main enzyme that metabolizes drugs, CPR, could serve a more complex role in AD.

Catalpol preserves neural function and attenuates the pathology of Alzheimer's disease in mice.

Alzheimer's disease (AD) is the most common form of dementia and there currently are no effective treatment strategies available. Catalpol is an iridoid glucoside, and large quantities can be isolated from the genus Rehmannia (Orobanchaceae). The present study assessed whether catalpol had any protective effects against Alzheimer's disease using a murine model. Reactive oxygen species (ROS)-associated enzymes as well as soluble Aß40 and Aß42 were detected using kits. Thioflavin­S staining was performed to detect senile plaques and reverse-transcription quantitative polymerase chain reaction was used to assess iroquois homeobox protein 3 (IRX3) and obesity­associated genes, while western blot analysis was used for ß­secretase 1 (BACE1), insulin­degrading enzyme (IDE) and neprilysin (NEP) detection. The Morris water maze was used to detect the learning ability and spatial memory. The results revealed that catalpol was able to reduce the oxidative stress in the cerebral cortex by regulating the activities and concentration of ROS­associated enzymes superoxide dismutase, glutathione peroxidase and catalase, however not malondialdehyde. Catalpol was also identified to be able to reduce the levels of soluble Aß40 and Aß42 in the cerebral cortex and thus inhibit the formation of senile plaques. These effects were observed to be regulated by IDE, however not by BACE1 or NEP. It is suggested that catalpol is not capable of directly regulating the expression of IRX3 and obesity­associated genes. Subsequent to the treatment with catalpol, impairments in learning and memory were also observed to be relieved using the Morris water maze test. The results of the present study indicate that catalpol may be a potential drug for the treatment of neurodegenerative diseases such as AD.

Complications and predictors associated with persistent hemodynamic depression after carotid artery stenting.

We aimed to investigate the complications and predictors associated with persistent hemodynamic depression (PHD) after carotid artery stenting (CAS). A total of 204 patients undergoing CAS in two centers between January 2011 and November 2013 were enrolled for study into two cohorts: PHD (systolic blood pressure <90 mm Hg and heart beat rate <60/min, which lasted more than 1h) and non-PHD according to their periprocedure detections. The complications were recorded and compared between the two groups. The predictors of PHD were analyzed by univariate analysis and logistic regression model. 43 patients developed PHD, which lasted for 17.22 h on average. The complications occurred in 9 patients of PHD group (angina pectoris 2, myocardial infarction 1, cerebral infarction 3, transient ischemic attack 2 and intestinal obstruction 1), which was significantly more than non- PHD group (angina pectoris 1, cerebral infarction 1, transient ischemic attack 5, p=0.001). Regression analysis revealed that diabetes, severe calcified plaque and a balloon dilation pressure of more than 8 atmospheres (atm) were the independent predictors for PHD after CAS. We concluded that PHD may be related to increased complications of CAS. Patients with diabetes, more severe calcified plaque and more balloon dilation pressure are more prone to develop PHD after CAS.

[Mathematical cognitive function in children with attention deficit hyperactivity disorder: a behavior and event-related potential study].

OBJECTIVE: To explore the mathematics cognitive function of children with attention deficit hyperactivity disorder and explore neural mechanisms with event-related potential(ERP) and behaviors. METHODS: Behavior data and ERP elicited by performing mental calculation tasks were recorded in 27 children with ADHD and 29 normal controls from July to October 2012 at Third Affiliated Hospital of Soochow University.The differences of behaviors and N2 component of ERP were compared and analyzed. RESULTS: The reaction time of the children with ADHD were longer than the control group in addition, subtraction and multiplication ((949 ± 144) vs (829 ± 166) ms, (981 ± 129) vs (856 ± 170) ms, (944 ± 136) vs (825 ± 172) ms, all P < 0.05). While the correct rate were less than normal control in all three arithmetic operations (0.80% (0.72%, 0.88%) vs 0.90% (0.85%,0.96%), 0.78% (0.64%,0.85%) vs 0.90% (0.84%,0.93%), 0.86% (0.74%,0.92%) vs 0.93%(0.90%,0.98%), all P < 0.05). N2 component could be elicited by all subjects in forehead. The amplitude of N2 of children with ADHD were significantly lower than control group in all three arithmetic operations at left frontal (F3: (-3.5 ± 5.2) vs (-6.7 ± 3.5)µV, (-3.8 ± 4.0) vs (-7.4 ± 4.5)µV, -5.8 (-7.6,1.6) vs -6.4(-10.3, -4.9) µV, all P < 0.05) and Fz ((-4.3 ± 6.4) vs ( -7.4 ± 4.2) µV, (-5.0 ± 5.4) vs (-7.9 ± 4.6)µV, -5.2(-9.7, -0.6) vs -7.9 (-10.5, -5.1)µV, all P < 0.05), the latency of ADHD group were prolonger than controls in subtraction operations at right and left frontal ((328 ± 36) vs (307 ± 27)ms, 325 (307,354)vs 309 (280, 330)ms) and frontal electrodes ((331 ± 35) vs (311 ± 30) ms, all P < 0.05). In addition and multiplication operations, there was no significant difference in latency (all P > 0.05). CONCLUSIONS: The children with ADHD have weak capacities of inhibition irrelevant information and paying attention to control. Their deficits in mental arithmetics may be due to the difficulties of selecting the best strategy during cognitive tasks.

[Changes of plasma fibrinogen level among acute ischemic stroke subtypes according to TOAST criteria and effects of Songling Xuemaikang].

OBJECTIVE: To investigate the changes of plasma fibrinogen level among acute ischemic stroke (ACI) subtypes according to Trial of Org10172 in Acute Stroke Treatment (TOAST) criteria and effects of Songling Xuemaikang. METHOD: The 160 patients with acute ischemic stroke were divided into two groups randomly: treatment group 85 cases (Songling Xuemaikang + Shuxuetong + Aspirin enterie coated tablets), control group 75 cases (Shuxuetong + Aspirin enterie ccoated tablets). The plasma fibrinogen was detected before and after treatment. RESULT: Compared with OC subtype, Fbg was higher in LAA, CE and SAO subtypes (P < 0.05). Compared with UE subtype, Fbg was higher in LAA, CE and SAO subtypes (P < 0.05). There was a significantly difference between LAA and SAO (P < 0.05). In LAA, SAO, CE of treatment group,the Fbg level were lowered significantly at the 15th day compared with pretherapy (P < 0.05). There was a significantly difference of Fbg between treatment group and control group In LAA, SAO and CE subtypes at the 15th day (P < 0.05). CONCLUSION: Fbg produces a marked effect at the pathomechanism of LAA, SAO and CE subtypes. Songling Xuemaikang can depress the plasma fibrinogen level of ACI, and be an effective adjunctive therapy on ACI.

dl-3-n-Butylphthalide prevents oxidative damage and reduces mitochondrial dysfunction in an MPP(+)-induced cellular model of Parkinson's disease.

The aim of the present study was to explore the neuroprotective effects and mechanisms of action of dl-3-n-butylphthalide (NBP) in a 1-methyl-4-phenylpyridiniumion (MPP(+))-induced cellular model of Parkinson's disease (PD). NBP was extracted from seeds of Apium graveolens Linn. (Chinese celery). MPP(+) treatment of PC12 cells caused reduced viability, formation of reactive oxygen, and disruption of mitochondrial membrane potential. Our results indicated that NBP reduced the cytotoxicity of MPP(+) by suppressing the mitochondrial permeability transition, reducing oxidative stress, and increasing the cellular GSH content. NBP also reduced the accumulation of alpha-synuclein, the main component of Lewy bodies. Given that NBP is safe and currently used in clinical trials for stroke patients, NBP will likely be a promising chemical for the treatment of PD.

Combination of autologous fascia lata and fat injection into the vocal fold via the cricothyroid gap for unilateral vocal fold paralysis.

OBJECTIVES: To apply the technique of injection of a combination of autologous fascia lata and fat into the vocal fold via the cricothyroid gap for unilateral vocal fold paralysis and to evaluate the therapeutic effect in 12 patients who underwent the procedure. DESIGN: Retrospective analysis of 12 patients. SETTING: Academic research. PATIENTS: A mixture of autologous fascia lata and fat was injected into the thyroarytenoid muscle of the paralyzed vocal fold in 12 patients. MAIN OUTCOME MEASURES: Videolaryngostroboscopy was performed to observe the changes to the vocal fold. The patients' phonatory function before and after surgery was assessed by computerized acoustic analysis and by blinded perceptual evaluation. RESULTS: Videolaryngostroboscopy demonstrated that the paralyzed vocal folds in these patients were pushed medially after the procedure. Statistically significant improvements were found in the perturbation measurements (jitter and shimmer), harmonics to noise ratio, and maximum phonation time. Ratings by a panel of voice experts also showed each voice to be statistically significantly improved after the procedure. No complications were noted. CONCLUSION: A combination of autologous fascia lata and fat injected into the vocal fold for unilateral vocal fold paralysis is a safe and effective therapy.

Development of 5-valent conjugate pneumococcal protein A - Capsular polysaccharide pneumococcal vaccine against invasive pneumococcal disease.

In this study, we synthesized a 5-valent pneumococcal conjugate vaccine, which was prepared with the pneumococcal capsular polysaccharides (PCPs) (from Streptococcus pneumoniae 1, 5, 6B, 19F, 23F) and pneumococcal surface protein A (PspA) mediated by 1,4-butanediol diglycidyl ether. The PspA cloned from serotype 19 strain showed good cross-immune response to 1, 5, 6B, and 23F serotypes of Streptococcus pneumonia (S. pneumoniae). Analysis of the maturation process of conjugate polyclonal antibody showed that conjugation with the protein carrier converted the polysaccharide from a weak T cell-independent (TI) antigen to a T cell-dependent (TD) antigen, although antibodies affinity to polysaccharide was not as strong as it to PspA in conjugate. We used an invasive disease mouse model to evaluate the protective efficacy of this conjugate vaccine. Active and passive protection against intraperitoneal challenge with virulent type 6B strain showed that the median survival times for mice immunized with conjugate were significantly longer than that of mice treated with capsular polysaccharides or PspA alone. Our study's results showed that immunization of the 5-valent PspA-capsular polysaccharides conjugate vaccine could afford strong protection to mice against the invasion of 1, 5, 6B, 19F, 23F serotypes S. pneumoniae.

Role of autophagy and proteasome degradation pathways in apoptosis of PC12 cells overexpressing human alpha-synuclein.

Parkinson's disease is a common neurodegenerative disease in the elderly. Its causes and mechanisms are not clearly understood. To explore the specific role of autophagy and the ubiquitin-proteasome pathway in apoptosis, a specific proteasome inhibitor and macroautophagy inhibitor and stimulator were selected to investigate pheochromocytoma (PC12) cell lines transfected with human mutant (A30P) and wild-type (WT) alpha-synuclein. The apoptosis ratio was assessed by flow cytometry. LC3, heat shock protein 70 (hsp70) and caspase-3 expression in cell culture were determined by Western blot. The hallmarks of apoptosis and autophagy were assessed with transmission electron microscopy. Compared to the control group or the rapamycin (autophagy stimulator) group, the apoptosis ratio in A30P and WT cells was significantly higher after treatment with inhibitors of the proteasome and macroautophagy. The results of Western blots for caspase-3 expression were similar to those of flow cytometry; hsp70 protein was significantly higher in the proteasome inhibitor group than in control, but in the autophagy inhibitor and stimulator groups, hsp70 was similar to control. These findings show that inhibition of the proteasome and autophagy promotes apoptosis, and the macroautophagy stimulator rapamycin reduces the apoptosis ratio. And inhibiting or stimulating autophagy has less impact on hsp70 than the proteasome pathway.

MPP+ impairs autophagic clearance of alpha-synuclein by impairing the activity of dynein.

Increasing evidence suggests that dynein has an important role in the clearance of misfolded proteins by autophagy. Here we show that treatment of cells with 1-methyl-4-phenylpyridinium (MPP) cause alpha-synuclein overexpression and aggregation, leading to the accumulation of autophagic vacuoles and the recruitment of LC3-II to these vacuoles in the cytoplasm. After MPP treatment, dynein expression decreased and was mainly aggregated at the periphery of cytoplasm and lost its colocalization with alpha-synuclein and lamp1, indicating that dynein lost its function in the aggresome formation and failed to return autophagosome and lysosomes to the center of the cell for degradation. We consider that dynein plays an important role in the autophagic clearance of aggregate-prone proteins.

Production of allogenic cartilage in a tube lined with epithelium and a novel scaffold.

OBJECTIVE: To study the feasibility of engineering cartilage tissue in a tube lined with epithelium and implanting allogenic chondrocytes in a novel scaffold that is made of chitosan nonwoven cloth coated with poly(DL-lactide-co-glycolide). DESIGN: Laboratory research. SUBJECTS: Allogenic chondrocytes were obtained from the auricles of 1-month-old New Zealand white rabbits. After the cells were cultured in vitro for 3 or 4 passages, they were implanted in the scaffolds to form composite grafts and then transplanted into the rabbits. After 6, 12, and 18 weeks, the general histologic characteristics were investigated. RESULTS: The cobweb-like matrix was observed approximately 1 week after the chondrocytes had been implanted in the scaffolds. At 6 weeks, the matrix was secreted, and there were immature chondrocytes in the grafts. At 12 weeks, the allogenic cartilage in the tube lined with epithelium had been created. Chondrocytes were almost mature and the lacunae had formed. At 18 weeks, the neocartilage was similar to native cartilage. CONCLUSION: It is feasible to produce allogenic cartilage in a tube lined with epithelium by implanting allogenic chondrocytes into a novel scaffold made of chitosan nonwoven cloth coated with poly(DL-lactide-co-glycolide).