Search PubMed⌕ Search

Biomedical subjects

Ying Zhao

Publications and source records attributed to Ying Zhao.

At least 19 recordsLinked to original sources

Identification of a novel and a recurrent CDC45 variant in a Chinese family with Meier-Gorlin syndrome 7 and a literature review.

INTRODUCTION: Meier-Gorlin syndrome 7 (MGORS7) is a rare autosomal recessive disorder characterized by primordial dwarfism, craniosynostosis, and patellar aplasia, caused by pathogenic variants of CDC45. Here, we report a Chinese patient presenting with classic hallmarks of MGORS7 alongside atypical clinical features, including hearing and visual impairments. METHODS: Clinical and radiological data were collected. Whole-genome sequencing and Sanger sequencing were performed to identify and validate the causative variants. Their functional effects were investigated using an exon-trapping assay, and a literature review of previously reported MGORS7 cases was conducted. RESULTS: Genetic analysis identified two compound heterozygous CDC45 variants: c.1416C>T (p.H472=) and c.1559+2T>A, which are a recurrent variant in the East Asian population and a novel variant, respectively. Our exon-trapping assay indicated that c.1559+2T>A induced aberrant splicing, generating transcripts predicted to undergo nonsense-mediated mRNA decay. Additionally, growth hormone therapy was initiated in our patient, with a noted improvement in growth parameters in the initial assessment and without immediate complications. The literature review identified a total of 32 CDC45 variants in 29 patients with MGORS7, who showed high heterogeneity in clinical phenotypes. DISCUSSION: Our study further expanded the mutational spectrum of CDC45 and provided a preliminary clinical observation suggesting that growth hormone therapy may be beneficial for growth retardation in patients with MGORS7.

CDC45↗

CAFs shape the immunosuppressive microenvironment of pancreatic cancer through the Lin28b-STING Axis.

Cancer-associated fibroblasts comprise diverse functionally distinct cellular subsets, with certain subpopulations exerting pivotal influence in shaping the pancreatic cancer immune microenvironment. Here we show that Lin28b+ cancer-associated fibroblasts contribute to establishing an immunologically cold tumor microenvironment in pancreatic ductal adenocarcinoma. Mechanistically, Lin28b directly binds to STING mRNA and promotes its degradation, thereby suppressing STING expression and downstream type I interferon signaling. Loss of Lin28b in cancer-associated fibroblasts activates the cGAS-STING-interferon signaling cascade, enhancing dendritic cell antigen presentation and CD8+ T cell cytotoxic function. Importantly, genetic inhibition of Lin28b in cancer-associated fibroblasts enhances sensitivity to anti-PD-L1 immune checkpoint blockade therapy. These findings reveal that targeting the Lin28b-STING axis represents a promising therapeutic strategy for overcoming the intrinsic resistance of pancreatic ductal adenocarcinoma to immunotherapy.

Humans↗

Context-dependent roles of DHX9 in Cancer: Molecular mechanisms, biomarker potential, and therapeutic perspectives.

DExH-box helicase 9 (DHX9) is a multifunctional nucleic acid helicase that participates in R-loop homeostasis, genome maintenance, RNA metabolism, and innate immune signaling. Accumulating evidence has linked aberrant DHX9 expression or activity to tumorigenesis, tumor progression, treatment response, and patient prognosis. However, its role in cancer is highly context-dependent, rather than uniformly oncogenic or tumor suppressive. Depending on its molecular partners, subcellular localization, post-translational modifications, tumor genotype, and immune microenvironment, DHX9 may either promote malignant phenotypes or contribute to tumor-restraining processes. In this review, we summarize the molecular characteristics and regulatory properties of DHX9, discuss its roles in genome stability, transcriptional and post-transcriptional control, circular RNA (circRNA) biogenesis, and tumor-immune crosstalk, and evaluate its emerging value as a potential biomarker and therapeutic target. We also highlight key challenges in this field, including mechanistic heterogeneity, insufficient translational validation, and the urgent need for context-informed patient stratification to maximize the clinical utility of DHX9-targeted strategies.

Humans↗

WDFY2 promotes MRN complex formation required for homologous recombination-mediated DNA repair.

The MRE11-RAD50-NBS1 (MRN) complex is fundamental for detecting and repairing DNA double-strand breaks (DSBs), thereby safeguarding genome integrity. However, the precise mechanism governing MRN complex recruitment to DSBs remains largely unexplored. Here, we identify WD40- and FYVE domain-containing protein 2 (WDFY2) as an important regulator of MRN complex formation at DNA damage sites, facilitating homologous recombination (HR) repair. Mechanistically, WDFY2 is phosphorylated at serine 84 by the ATM-CHK2 axis, priming it for recruitment to DSBs. Through direct interactions with MRE11 and NBS1, WDFY2 bridges the MRE11-RAD50 subcomplex with NBS1, thereby promoting MRN complex formation at DSBs and DNA end resection. WDFY2 deficiency, as well as the non-phosphorylatable S84A mutant, results in impaired HR repair and reduced cell survival following DNA damage. Collectively, our findings establish WDFY2 as a key platform for MRN complex loading at DSBs and HR repair, highlighting it as a potential therapeutic target for cancer treatment.

Humans↗

TPX2 promotes papillary renal cell carcinoma progression by forming a ceRNA with LINC00894.

PURPOSE: Papillary renal cell carcinoma (pRCC), particularly type 2, is associated with a poor prognosis. This study aimed to identify molecular mechanisms underlying pRCC progression and explore potential therapeutic targets to improve patient outcomes. METHODS: TPX2 expression was analyzed in tumor samples from patients with type 2 pRCC. In vitro experiments were conducted to assess the effects of TPX2 and LINC00894 knockdown and overexpression on the proliferation and migration of Caki-2 and ACHN cells. Immunohistochemical analysis of tissue microarrays was performed to evaluate the associations between TPX2 expression and clinicopathological characteristics in type 2 pRCC patients. RESULTS: Elevated TPX2 expression was significantly associated with a worse prognosis in type 2 pRCC patients and served as an independent risk factor for overall survival. Knockdown of TPX2 in Caki-2 and ACHN cells significantly reduced cell proliferation and migration. Additionally, LINC00894 was highly expressed in type 2 pRCC and correlated with poor prognosis. Mechanistically, miR-660-5p targeted the TPX2 3' UTR, promoting TPX2 degradation, while LINC00894 competitively bound to miR-660-5p, protecting TPX2 from miRNA-mediated degradation and exerting a pro-oncogenic effect. Immunohistochemical analysis revealed significant correlations between TPX2 expression and clinicopathological features, including tumor thrombus volume, tumor diameter, pathological TNM stage, and Fuhrman grade. CONCLUSION: This study underscores the critical role of TPX2 in type 2 pRCC progression and highlights its potential as a prognostic biomarker and therapeutic target. The TPX2/LINC00894/miR-660-5p regulatory axis provides novel insights into the molecular mechanisms driving pRCC and offers a promising avenue for improving patient prognosis.

Humans↗

The 13-lipoxygenase GmLOX6 is involved in JA biosynthesis and serves as a positive regulator of salt stress tolerance in soybean.

Salinity represents a major abiotic stressor that significantly impairs soybean growth and yield. Although jasmonic acid (JA) has been firmly established as a key regulator of plant defense against salt stress, the precise functions of lipoxygenase (LOX) genes responsible for initiating JA biosynthesis remain poorly defined. Here, a comprehensive genome-wide analysis of the soybean LOX gene family was performed, and a detailed functional characterization of GmLOX6 was carried out. Subcellular localization confirmed that GmLOX6 is targeted to chloroplasts, while enzymatic assays demonstrated that it acts as a 13-LOX enzyme with a strong preference for α-linolenic acid as substrate. To clarify its role under salt stress, we generated both overexpression and CRISPR/Cas9-mediated knockout lines of soybean. Phenotypic and molecular evaluations revealed that GmLOX6 facilitates JA production under salt stress, thereby contributing to enhanced JA accumulation. This elevation in JA levels was associated with improved salt tolerance through multiple physiological adaptations, including the activation of antioxidant enzymes for the detoxification of reactive oxygen species (ROS), enhanced Na+ extrusion to preserve ionic balance, and reinforced membrane stability. Moreover, GmRWP-RK11 was identified as a transcriptional repressor of GmLOX6. Functional disruption of GmRWP-RK11 via CRISPR/Cas9 conferred greater salt tolerance, further supporting its negative regulatory role. Collectively, these findings uncover a novel regulatory axis in which GmLOX6-mediated JA biosynthesis enhances soybean resistance to salinity through modulation of ROS homeostasis and Na+ transport. These insights provide an expanded understanding of the transcriptional and biochemical mechanisms underpinning JA-driven stress adaptation in soybean.

Glycine max↗

Protective effect of glycyrrhizin, glycyrrhetic acid and matrine on acute cholestasis induced by alpha-naphthyl isothiocyanate in rats.

Alpha-naphthyl isothiocyanate (ANIT) is a known hepatotoxicant that causes acute cholestatic hepatitis characterized by the infiltration of neutrophils around bile ducts and necrotic hepatocytes. The effects of glycyrrhizin (GL), 18beta-glycyrrhetinic acid (GA), matrine (MT), oxymatrine (OMT), salvianolic acid B (SAB), silymarin (SI) and dexamethasone (DEX) on ANIT-induced acute cholestasis in rats were investigated. Serological and histological data demonstrated that the administration of GL, GA or MT all protected against hepatocyte injury and cholestasis induced by ANIT. Furthermore, the bile flow and the accumulative bile excretion of ketoprofen glucuronide (KPG), that were significantly suppressed by ANIT, were preserved in rats administered GL, GA or MT. DEX protected against acute cholestasis but did not protect against hepatocyte necrosis and elevated serum alanine aminotransferase levels following ANIT administration. Rats administrated OMT, SAB or SI were not resistant to ANIT toxicity. In summary, the protective effect of DEX is directed toward cholangiocytes rather than hepatocytes whereas the natural products, GA, GL and MT, exhibit significantly better protective effects against ANIT-induced liver damage including the protection of hepatocytes as well as cholangiocytes.

Acute Disease↗

Transduction of beta3 integrin subunit cDNA confers on human keratinocytes the ability to adhere to gelatin.

alphavbeta3 is a multiligand integrin receptor that interacts with fibrinogen (FG), fibrin (FB), fibronectin (FN), vitronectin (VN), and denatured collagen. We previously reported that cultured normal human keratinocytes, like in vivo keratinocytes, do not express alphavbeta3 on the cell surface, and do not adhere to and migrate on FG and FB. Furthermore, we reported that human keratinocytes transduced with beta3 integrin subunit cDNA by a retrovirus-mediated transduction method express alphavbeta3 on the cell surface and adhere to FG, FB, FN, and VN significantly compared with beta-galactosidase (beta-gal) cDNA-transduced keratinocytes (control). In this study, we determined whether these beta3 integrin subunit cDNA-transduced keratinocytes or normal human keratinocytes adhere to denatured collagen (gelatin) using a 1 h cell adhesion assay. beta3 cDNA-transduced keratinocytes adhered to gelatin, whereas no significant adhesion was observed with the control cells (beta-gal cDNA-transduced keratinocytes and normal human keratinocytes). The adhesion to gelatin was inhibited by LM609, a monoclonal antibody to alphavbeta3, and RGD peptides but not by normal mouse IgG1 nor RGE peptides. Thus, transduction of beta3 integrin subunit cDNA confers on human keratinocytes the ability to adhere to denatured collagen (gelatin) as well as to FG, FB, VN, and FN. Otherwise, normal human keratinocytes do not adhere to gelatin. These data support the idea that beta3 cDNA-transduced human keratinocytes can be a good material for cultured epithelium to achieve better take rate with acute or chronic wounds, in which FG, FB, and denatured collagen are abundantly present.

Antibodies, Monoclonal↗

Ketoprofen glucuronidation and bile excretion in carbon tetrachloride and alpha-naphthylisothiocyanate induced hepatic injury rats.

A pharmacokinetic study was carried out in rats to investigate the effects of experimental hepatic injury on the liver glucuronidation and bile excretion of ketoprofen (KP) and its glucuronides (KPGs). In vivo, KP (20mg/kg b.w.) was intravenously administered to carbon tetrachloride (CCl(4)) or alpha-naphthylisothiocyanate (ANIT) induced hepatic injury male rats. Concentrations of KP and its glucuronides (S-KPG and R-KPG) in plasma and bile were determined by RP-HPLC. It was observed that there was significant difference in the accumulative bile excretion of KPGs between the CCl(4) intoxicated rats and the normal rats (54+/-18.3% versus 90+/-6.9%), while it was extremely inhibited in ANIT intoxicated rats (2.0+/-3.1% versus 90+/-6.9%). As the result of reduction of KPGs excreted in bile, the area under the curve (AUC((0-infinity))) of KP and KPGs were higher in blood in CCl(4) and ANIT hepatic injury rats than those of the normal rats. Specifically, ANIT caused approximately 10-fold elevation of AUC((0-infinity)) of plasma S-KPG. In microsomal incubations experiment, the glucuronyltransferase activity was impaired in CCl(4) and ANIT intoxicated rats. It suggested that the glucuronyltransferase activity was impaired in CCl(4) and ANIT intoxicated rats, while the bile excretion function was suppressed extremely in ANIT intoxicated rats.

Alanine Transaminase↗

Crystallization behaviors of n-nonadecane in confined space: observation of metastable phase induced by surface freezing.

Crystallization and phase transition behaviors of n-nonadecane in microcapsules with a diameter of about 5 mum were studied with the combination of differential scanning calorimetry (DSC) and synchrotron radiation X-ray diffraction (XRD). As evident from the DSC measurement, a surface freezing monolayer, which is formed in the microcapsules before the bulk crystallization, induces a novel metastable rotator phase (R(II)), which has not been reported anywhere else. We argue that the existence of the surface freezing monolayer decreases the nucleating potential barrier of the R(II) phase and induces its appearance, while the lower free energy in the confined geometry turns the transient R(II) phase to a "long-lived" metastable phase.

Journal Article↗

Novel link between E2F1 and Smac/DIABLO: proapoptotic Smac/DIABLO is transcriptionally upregulated by E2F1.

Deregulated expression of E2F1 not only promotes S-phase entry but also induces apoptosis. Although it has been well documented that E2F1 is able to induce p53-dependent apoptosis via raising ARF activity, the mechanism by which E2F induces p53-independent apoptosis remains unclear. Here we report that E2F1 can directly bind to and activate the promoter of Smac/DIABLO, a mitochondrial proapoptotic gene, through the E2F1-binding sites BS2 (-542 approximately -535 bp) and BS3 (-200 approximately -193 bp). BS2 and BS3 appear to be utilized in combination rather than singly by E2F1 in activation of Smac/DIABLO. Activation of BS2 and BS3 are E2F1-specific, since neither E2F2 nor E2F3 is able to activate BS2 or BS3. Using the H1299 ER-E2F1 cell line where E2F1 activity can be conditionally induced, E2F1 has been shown to upregulate the Smac/DIABLO expression at both mRNA and protein levels upon 4-hydroxytamoxifen treatment, resulting in an enhanced mitochondria-mediated apoptosis. Reversely, reducing the Smac/DIABLO expression by RNA interference significantly diminishes apoptosis induced by E2F1. These results may suggest a novel mechanism by which E2F1 promotes p53-independent apoptosis through directly regulating its downstream mitochondrial apoptosis-inducing factors, such as Smac/DIABLO.

Apoptosis↗

Ghrelin acts on the dorsal vagal complex to stimulate pancreatic protein secretion.

Ghrelin receptors are present in the central nervous system. We hypothesized that ghrelin released from the stomach acts as an endocrine substance and stimulates brain stem vagovagal circuitry to evoke pancreatic secretion. In an in vivo anesthetized rat model, an intravenous infusion of ghrelin at doses of 5, 10, and 25 nmol increased pancreatic protein secretion from a basal level of 125 +/- 6 to 186 +/- 8, 295 +/- 12, and 356 +/- 11 mg/h, respectively. Pretreatment with atropine or hexamethonium or an acute vagotomy, but not a perivagal application of capsaicin, completely abolished pancreatic protein secretion responses to ghrelin. In conscious rats, an intravenous infusion of ghrelin at a dose of 10 nmol resulted in a 2.2-fold increase in pancreatic protein secretion over basal volume. Selective ablation of the area postrema abolished pancreatic protein secretion stimulated by intravenous infusion of ghrelin but did not alter the increase in pancreatic protein secretion evoked by diversion of bile-pancreatic juice. Immunohistochemical staining showed a marked increase in the number of c-Fos-expressing neurons in the area postrema, nucleus of the solitary tract, and dorsal motor nucleus of the vagus after an intravenous infusion of ghrelin in sham-lesioned rats; selective ablation of the area postrema eliminated this increase. In conclusion, ghrelin stimulates pancreatic secretion via a vagal cholinergic efferent pathway. Circulating ghrelin gains access to the brain stem vagovagal circuitry via the area postrema, which represents the primary target on which peripheral ghrelin may act as an endocrine substance to stimulate pancreatic secretion.

Animals↗

Molecular dynamics simulation studies of a protein-RNA complex with a selectively modified binding interface.

The RNA recognition motif (RRM) is one of the most common RNA binding domains. We have investigated the contribution of three highly conserved aromatic amino acids to RNA binding by the N-terminal RRM of the U1A protein. Recently, we synthesized a modified base (A-4CPh) in which a phenyl group is tethered to adenine using a linker of 4 methylene groups. The substitution of this base for adenine in the target RNA selectively stabilizes the complex formed with a U1A protein in which one of the conserved aromatic amino acids is replaced with Ala (Phe56Ala). In this article, we report molecular dynamics (MD) simulations that probe the structural consequences of the substitution of A-4CPh for adenine in the wild type and Phe56Ala U1A-RNA complexes and in the free RNA. The simulations suggest that A-4CPh stabilizes the complex formed with Phe56Ala by adopting a folded conformation in which the tethered phenyl group fills the site occupied by the phenyl group of Phe56 in the wild-type complex. In contrast, an extended conformation of A-4CPh is predicted to be most stable in the complex formed with the wild-type protein. The calculations indicate A-4CPh is in an extended conformation in the free RNA. Therefore, preorganizing the structure of the phenyl-tethered base for binding may improve both the affinity and specificity of the RNA containing A-4CPh for the Phe56Ala U1A protein. Taken together, the previous experimental work and the calculations reported here suggest a general design strategy for altering RRM-RNA complex stability.

Computer Simulation↗

Nitric oxide suppresses EPO-induced monocyte chemoattractant protein-1 in endothelial cells: implications for atherogenesis in chronic renal disease.

Patients with advanced chronic renal disease (CRD) suffer from excessive morbidity and mortality due to complications of accelerated atherosclerosis. Approximately 90% of dialysis-dependent end stage renal disease patients suffer from anemia. Recombinant human erythropoietin (EPO) in combination with iron has become widely used to treat anemic CRD patients. While treatment with EPO results in improved quality of life it may also contribute to the development of atherosclerosis. Recent studies suggest that a reduction in nitric oxide (NO) availability may be linked to EPO-induced vascular dysfunction. Furthermore, CRD per se is thought to result in a state of NO deficiency. The present study suggests that EPO may exert proatherogenic activity by augmenting the cytokine-induced expression of monocyte-chemoattractant protein-1 (MCP-1) in human umbilical vein endothelial cells (HUVECs) and by stimulating the proliferation of HUVECs and human vascular smooth muscle cells (HVSMCs). Augmentation of MCP-1 expression appears to be linked to EPO-induced downregulation of endothelial NO synthase (ecNOS). NO released from a series of synthetic donor compounds suppressed the EPO-mediated augmentation of cytokine-induced MCP-1 expression. In vitro studies revealed that EPO reduces ecNOS expression at both the protein and mRNA levels and that EPO also mediates a reduction in ecNOS enzymatic activity. These observations suggest potential mechanisms through which EPO may contribute to the development of accelerated atherosclerosis, particularly in the setting of CRD where NO availability may already be compromised.

Atherosclerosis↗

A novel model of acute liver injury in mice induced by T cell-mediated immune response to lactosylated bovine serum albumin.

The present study aimed to establish a murine liver injury model with T cell-mediated immune response to mimic the cellular immunological pathogenesis of hepatitis. Bovine serum albumin was conjugated with lactose by redox to prepare lactosylated bovine serum albumin (LacBSA). The liver injury was induced in C57BL/6 mice by a T cell-mediated immune response to LacBSA. After a systemic injection of LacBSA, which elicited immune response in mice sensitized twice with LacBSA, liver injury was observed with obvious increase of aminotransferase levels in serum and hepatocelluar damage in liver histology. However, the splenectomy before the elicitation significantly alleviated the liver injury. Direct contact between spleen T cells/nonparenchymal cells and hepatocytes was proved to be essential to induce the release of alanine aminotransferase in the culture supernatant. In addition, both levels of Fas mRNA in liver tissues and Fas Ligand in spleen cells were up-regulated at 6 h after the elicitation. The Fas mRNA expression was maintained in a relatively high level at 18 h while Fas Ligand began to decrease after 12 h. These results demonstrated that the T cell immune response to LacBSA could be successfully localized in the liver to induce an immunological liver injury in mice. The pathogenesis of the liver injury might involve the interaction between the liver-infiltrating lymphocytes and hepatocytes through Fas/FasL pathway.

Acute Disease↗

Evaluation of three different histamine concentrations in intradermal testing of normal cats and attempted determination of 'irritant' threshold concentrations for 48 allergens.

The purpose of this study was to determine the optimal histamine concentration and 'irritant' allergen threshold concentrations in intradermal testing (IDT) in normal cats. Thirty healthy cats were tested with three different histamine concentrations and four different concentrations of each allergen. The optimal histamine concentration was determined to be 1: 50,000 w/v (0.05 mg mL(-1)). Using this histamine concentration, the 'irritant' threshold concentration for most allergens was above the highest concentrations tested (4,000 PNU mL(-1) for 41 allergens and 700 PNU mL(-1) for human dander). The 'irritant' threshold concentration for flea antigen was determined to be 1:750 w/v. More than 10% of the tested cats showed positive reactions to Dermatophagoides farinae, Dermatophagoides pteronyssinus, housefly, mosquito and moth at every allergen concentration, which suggests that the 'irritant' threshold concentration for these allergens is below 1,000 PNU mL(-1), the lowest allergen concentration tested. Our results confirm previous studies in indicating that allergen and histamine concentrations used in feline IDT may need to be revised.

Allergens↗

Acetylation of p53 at lysine 373/382 by the histone deacetylase inhibitor depsipeptide induces expression of p21(Waf1/Cip1).

Generally, histone deacetylase (HDAC) inhibitor-induced p21(Waf1/Cip1) expression is thought to be p53 independent. Here we found that an inhibitor of HDAC, depsipeptide (FR901228), but not trichostatin A (TSA), induces p21(Waf1/Cip1) expression through both p53 and Sp1/Sp3 pathways in A549 cells (which retain wild-type p53). This is demonstrated by measuring relative luciferase activities of p21 promoter constructs with p53 or Sp1 binding site mutagenesis and was further confirmed by transfection of wild-type p53 into H1299 cells (p53 null). That p53 was acetylated after depsipeptide treatment was tested by sequential immunoprecipitation/Western immunoblot analysis with anti-acetylated lysines and anti-p53 antibodies. The acetylated p53 has a longer half-life due to a significant decrease in p53 ubiquitination. Further study using site-specific antiacetyllysine antibodies and transfection of mutated p53 vectors (K319/K320/K321R mutated and K373R/K382R mutations) into H1299 cells revealed that depsipeptide specifically induces p53 acetylation at K373/K382, but not at K320. As assayed by coimmunoprecipitation, the K373/K382 acetylation is accompanied by a recruitment of p300, but neither CREB-binding protein (CBP) nor p300/CBP-associated factor (PCAF), to the p53 C terminus. Furthermore, activity associated with the binding of the acetylated p53 at K373/K382 to the p21 promoter as well as p21(Waf1/Cip1) expression is significantly increased after depsipeptide treatment, as tested by chromatin immunoprecipitations and Western blotting, respectively. In addition, p53 acetylation at K373/K382 is confirmed to be required for recruitment of p300 to the p21 promoter, and the depsipeptide-induced p53 acetylation at K373/K382 is unlikely to be dependent on p53 phosphorylation at Ser15, Ser20, and Ser392 sites. Our data suggest that p53 acetylation at K373/K382 plays an important role in depsipeptide-induced p21(Waf1/Cip1) expression.

Acetylation↗

[Effects of Tongluo recipe on experimental diabetic peripheral neuropathy in rats].

OBJECTIVE: To investigate the effects of Tongluo Recipe (TLR), a compound Chinese herbal medicine, on experimental diabetic peripheral neuropathy in rats. METHODS: Diabetes was induced by streptozocin in rats. Eight weeks later, the diabetic rats were assigned to 3 groups according to different body weights: untreated group, low-dose TLR-treated group and high-dose TLR-treated group. Eight normal rats were assigned to normal control group. Systemic and sciatic nerve intrinsic antioxidant enzyme activities, lipid peroxide levels, hemorheology and sciatic nerve conduction velocity and ultrastructure changes were evaluated. RESULTS: Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities were lower, and lipid peroxide levels were higher in plasma and sciatic nerve of the untreated group than those in the normal control group (P<0.05). Blood glucose and viscosity in the untreated group were higher than those in the normal control group. Sciatic nerve showed demyelination changes and decrease of conduction velocity. Vasa nervorum expanded and erythrocyte deposited in the capillary in the untreated group. TLR obviously improved sciatic nerve conduction velocity and ameliorated morphology changes, decreased blood viscosity, improved SOD and GSH-Px activities. CONCLUSION: TLR can obviously improve sciatic nerve function and ameliorate morphology changes in rats with diabetic peripheral neuropathy, probably through depleting free radical production, improving endothelial cell function and ameliorating hemorheology changes.

Animals↗