Risk factors of prognosis in older patients with severe brain injury after surgical intervention.

BACKGROUND: Older patients (aged ≥ 60 years) with severe brain injury have a high mortality and disability rate. The objective of this retrospective study was to assess the clinical risk factors of prognosis in older patients with severe brain injury after surgical intervention and to analyze the prognosis of the surviving group of patients 1 year after discharge. METHODS: Clinical data of older patients with severe brain injury who were admitted to two neurosurgical centers between January 2010 and December 2020 were collected. Patient age, sex, Glasgow Coma Scale (GCS) score at admission, underlying disease, mechanisms of injury, abnormal pupillary reflex, head computed tomography imaging findings (such as hematoma type),intraoperative brain swelling and other factors were reviewed. All the patients were categorized into a good prognosis (survival) group and a poor prognosis (death) group by the Glasgow Outcome Score (GOS); also, the related factors affecting the prognosis were screened and the independent risk factors were identified by the Binary logistic regression analysis. GOS was used to evaluate the prognosis of the surviving group of patients 1 year after discharge. RESULTS: Out of 269 patients, 171 (63.6%) survived, and 98 (36.4%) died during hospitalization. Univariate analysis showed that age, GCS score at admission, underlying diseases, abnormal pupillary reflex, the disappearance of ambient cistern, the midline structure shift, intraoperative brain swelling, oxygen saturation < 90%, and cerebral hernia were risk factors for the prognosis of older patients with severe brain injury after surgical intervention. Multivariate analysis showed that age, underlying diseases, disappearance of ambient cistern, Oxygen saturation < 90% and intraoperative brain swelling were independent risk factors of the prognosis in the population. The effect of surgical intervention differed among various age groups at 1-year follow-up after surgery. CONCLUSIONS: The results of this retrospective study confirmed that age, underlying diseases, disappearance of ambient cistern, intraoperative brain swelling, and oxygen saturation < 90% are associated with poor prognosis in older postoperative patients with severe brain injury. Surgical intervention may improve prognosis and reduce mortality in older patients (age < 75 years). But for those patients (age ≥ 75 years), the prognosis was poor after surgical intervention.

The efficacy and safety of several interventions of corticosteroids for CRSwNP patients after endoscope sinus surgery: A protocol for systematic review and network meta-analysis.

BACKGROUND: Corticosteroid has been a mainstay of chronic rhinosinusitis with nasal polyps (CRSwNP) medical therapy. While endoscopic sinus surgery (ESS) will be performed when patients had failed to respond to maximal medical therapy. Many studies shown that several corticosteroids of interventions (e.g., nasal spray, oral, atomization/nebulization, nasal irrigation, direct infiltration, and steroid-eluting stent, etc) have each demonstrated significant efficacy compared with placebo or no corticosteroids intervention except intranasal corticosteroids for the treatment of CRSwNP after ESS. The aim of this systematic review and network meta-analysis is to answer the following question: which 1 is the best corticosteroid of intervention for CRSwNP patients after ESS? METHODS: A systematic review will be conducted to identify studies involving randomized controlled trials which compared several different interventions of corticosteroids (e.g., nasal spray, oral, atomization/nebulization, nasal irrigation, direct infiltration, steroid-eluting stent, etc) for CRSwNP patients after ESS. The primary outcomes are efficacy (e.g., effective rate or cure rate), visual analogic scale of symptom severity, Lund-Kennedy endoscopic score, adverse events, and so on. We will comprehensively search PubMed, Embase, Cochrane Library, ClinicalTrials.gov, Web of Science, Chinese National Knowledge Infrastructure, Wangfang and VIP journal database from inception to July, 2022. For studies which meet our inclusion criteria, 2 reviewers will extract data independently and assess the quality of literature using a revision of version 2 of the Cochrane risk of bias tool (RoB 2.0). A random effects model will be used for all pairwise meta-analyses (with a 95% confidence interval). Network meta-analyses will be conducted to generate estimates of comparative effectiveness of each intervention class and rankings of their effectiveness. RESULTS: The results of this study expect to provide a high-quality, evidence-based recommendation on which 1 is the best corticosteroid of intervention for CRSwNP patients after ESS? DISCUSSION: This study will provide evidence regarding the comparability of several interventions of corticosteroids for CRSwNP patients after ESS. Also, the data generated from this review will provide health-care providers with a clear evidence synthesis of CRSwNP patients after ESS management strategies. These data will be incorporated into the development of a patient decision aid to assist patients and clinicians in making a preference-based decision when faced with a CRSwNP patients after ESS as well.

Autophagy Promotes Microglia Activation Through Beclin-1-Atg5 Pathway in Intracerebral Hemorrhage.

Previous study demonstrates that intracerebral hemorrhage (ICH) promotes microglia activation and inflammation. However, the exact mechanism of microglia activation induced by ICH is not clear. In this experiment, microglia autophagy was examined using electron microscopy, conversion of light chain 3(LC3), and monodansylcadaverine (MDC) staining to detect autophagic vacuoles. We found that ICH induced microglia autophagy and activation. The suppression of autophagy using either pharmacologic inhibitors (3-methyladenine, bafilomycin A1) or RNA interference in essential autophagy genes (BECN1 and ATG5) decreased the microglia activation and inflammation in ICH. Moreover, autophagy inhibitors reduced brain damage in ICH. In conclusion, these data indicate that ICH contributes to microglia autophagic activation through BECN1 and ATG5 and provide the therapeutical strategy for ICH.

Scavenger receptor SRA attenuates TLR4-induced microglia activation in intracerebral hemorrhage.

Scavenger receptor A (SRA) has been shown to participate in the pattern recognition of pathogen infection. However, its role in intracerebral hemorrhage has not been well defined. In this study, we detected SRA and TLR4 expression and inflammatory response of microglia treated with erythrocyte lysate in vitro, and observed the cerebral water content and neurological deficit of ICH mice in vivo. We found that SRA deficiency leads to greater sensitivity to erythrocyte lysate-induced inflammatory response. SRA down-regulated inflammatory response expression in microglia by suppressing TLR4-induced activation. Collectively, we have identified the molecular linkage between SRA and the TLR4 signaling pathways in ICH. And our results reveal that SRA has important clinical implications for TLR-targeted immunotherapeutical strategy in ICH.

MicroRNA367 negatively regulates the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage.

BACKGROUND: Intracerebral hemorrhage (ICH) induces microglial activation and the release of inflammatory cytokines, leading to inflammation in the brain. IRAK4, an essential component of the MyD88-dependent pathway, activates subsets of divergent signaling pathways in inflammation. METHODS: In the experiment, microglia were stimulated with erythrocyte lysates, and then miR-367, IRAK4, NF-ĸB activation and downstream proinflammatory mediator production were analyzed. In addition, inflammation, brain edema, and neurological functions in ICH mice were also assessed. RESULTS: Here, we report that ICH downregulated miR-367 expression but upregulated IRAK4 expression in primary microglia. We also demonstrate that miR-367 suppressed IRAK4 expression by directly binding its 3'-untranslated region. MiR-367 inhibited NF-ĸB activation and downstream proinflammatory mediator production. Knocking down IRAK4 in microglia significantly decreased the IRAK4 expression and inhibited the NF-ĸB activation and the downstream production of proinflammatory mediators. In addition, our results indicate that miR-367 could inhibit expression of proinflammatory cytokines, reduce brain edema, and improve neurological functions in ICH mice. CONCLUSIONS: In conclusion, our study demonstrates that miR-367/IRAK4 pathway plays an important role in microglial activation and neuroinflammation in ICH. Our finding also suggests that miR-367 might represent a potential therapeutic target for ICH.

Recombinant adenovirus encoding NLRP3 RNAi attenuate inflammation and brain injury after intracerebral hemorrhage.

Numerous evidence have shown that microglia mediated inflammation plays a pivotal role in the development of brain injury after intracerebral hemorrhage (ICH). Therefore anti-inflammation therapy represents a potentially promising approach to ICH. Recently, NLRP3 inflammasome was discovered to facilitate the inflammatory response. However, the effect of NLRP3 inflammasome after ICH has not been fully studied. To explore the potential of NLRP3 inflammasome, we detected NLRP3 expression, inflammation, brain edema and neurological functions in vitro and in vivo. We found that ICH activated the NLRP3 inflammasome and inflammation. However, NLRP3 RNAi could attenuate inflammation and brain injury after ICH. Therefore, the findings suggested that recombinant adenovirus encoding NLRP3 RNAi might be valuable as a potential strategy for anti-inflammation therapy in ICH.

A novel nanoparticle containing neuritin peptide with grp170 induces a CTL response to inhibit tumor growth.

Malignant glioma is among the most challenging of all cancers to treat successfully. Despite recent advances in surgery, radiotherapy and chemotherapy, current treatment regimens have only a marginal impact on patient survival. In this study, we constructed a novel nanoparticle containing neuritin peptide with grp170. The nanoparticle could elicit a neuritin-specific cytotoxic T lymphocyte response to lyse glioma cells in vitro. In addition, the nanoparticle could inhibit tumor growth and improve the lifespan of tumor-bearing mice in vivo. Taken together, the results demonstrated that the nanoparticle can inhibit tumor growth and represents a promising therapy for glioma.

Toll-like receptor-4-mediated autophagy contributes to microglial activation and inflammatory injury in mouse models of intracerebral haemorrhage.

AIMS: Much evidence demonstrates that Toll-like receptor-4 (TLR4)-mediated microglial activation is an important contributor to the inflammatory injury in intracerebral haemorrhage (ICH). However, the exact mechanism of TLR4-mediated microglial activation induced by ICH is not clear. In addition, microglial autophagy is involved other forms of nervous system injury. To explore the relationship between TLR4 and autophagy, we investigated the role of TLR4-mediated microglial autophagy and inflammation in ICH. METHODS: We detected TLR4 expression, autophagy and inflammation of microglia treated with lysed erythrocytes in vitro, and observed the cerebral water content and neurological deficit of ICH mice [TLR4-/- and wild type (WT)] in vivo. RESULTS: We found that lysed erythrocyte treated microglia (TLR4-/-) had reduced autophagy and inflammation compared with microglia (WT) in vitro. ICH mice (TLR4-/-) had reduced water content and neurological injury compared with ICH mice (WT). The autophagy inhibitor (3-methyladenine) decreased microglial activation and inflammatory injury due to lysed erythrocyte treatment, and improved the neurological function of ICH mice. CONCLUSIONS: Taken together, these data suggested that TLR4 induced autophagy contributed to the microglial activation and inflammatory injury and might provide novel therapeutic interventions for ICH.

Scavenger receptor SRA attenuates microglia activation and protects neuroinflammatory injury in intracerebral hemorrhage.

Microglia mediated neuroinflammation plays a crucial role in intracerebral hemorrhage (ICH). Therefore, the negative feedback immune mechanism to keep microglia homeostasis and inhibit the related inflammatory injury is important. Scavenger receptor A (SRA), a pattern recognition molecule, is a physiologic negative regulator of immune consequences. However, its role in microglia mediated immune response has not been well defined. In this study, we detected SRA expression and inflammatory response of microglia treated with erythrocyte lysate in vitro, and observed the cerebral water content and neurological deficit of ICH mice in vivo. We found that SRA was highly expressed in erythrocyte lysate treated microglia. Interestingly, genetic SRA ablation increased microglia activation and cytokine production, and sensitized mice to ICH induced neuron injury. In addition, we adoptive transferred microglia (WT) into ICH mice (SRA-/-), and found that the ICH-induced inflammation injury was effectively ameliorated. Therefore, the results demonstrated that SRA could attenuate microglia mediated inflammation injury in ICH. In addition, SRA mediated negative feedback mechanism in neuroimmune homeostasis might provide a novel therapeutical strategy for ICH. Scavenger receptor SRA restrains T cell activation and protects against concanavalin A-induced hepatic injury.

Regulatory T cells inhibit microglia activation and protect against inflammatory injury in intracerebral hemorrhage.

Numerous evidence demonstrate that microglia mediated inflammatory injury plays a critical role in intracerebral hemorrhage (ICH). Therefore, the way to inhibit the inflammatory response is greatly needed. Treg cells have been shown to play a critical role in immunologic self-tolerance as well as anti-tumor immune responses and transplantation. In the current study, we transfered Treg cells in the ICH model, and investigated the effect. The cytokines of microglia were measured by ELISA, JNK/ERK and NF-κB were measured by Western blot and EMSA (Electrophoretic Mobility Shift Assay), animal behavior was evaluated by animal behavioristics. We found that Treg cells could inhibit microglia mediated inflammatory response through NF-κB activation via the JNK/ERK pathway in vitro, and improve neurological function in vivo. Our findings suggest that Treg cells could suppress inflammatory injury and represent a novel cell-based therapeutical strategy in ICH.

Dendritic cells transduced with CPEB4 induced antitumor immune response.

Much evidence leads to the exploration of immunologic approaches for eliminating tumor cells. Cytoplasmic polyadenylation element binding protein 4 (CPEB4) is considered to be a novel therapeutical target for glioblastoma. In this study, we transduced DCs with CPEB4 to explore the immune response in vivo. We found that DCs transduced with recombinant adenovirus encoding CPEB4 could induce specific cytotoxic T lymphocytes (CTLs) to lyse glioma cells and augment the number of IFN-γ secreting T-cells in mice. In addition, the modified DCs could effectively protect mice from lethal challenges against glioma cells, reduce tumor growth and increase the mice life span. These results suggest that the DC transduced with CPEB4 may induce anti-tumor immunity against glioma cells and might be used as an efficient tumor vaccine in clinical applications.

Sinomenine inhibits microglia activation and attenuates brain injury in intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) causes morbidity and mortality and commonly follows the reperfusion after an ischemic event. Microglial activation mediated cytokine and protease secretion contributes to brain injury in ICH. Previous studies have shown that sinomenine possesses potent immunoregulatory properties. However, little is known about its exact role in ICH. In the present study, to investigate the effect of sinomenine on microglial cells inflammation, we treated ICH-challenged BV2 microglial cells with sinomenine in vitro, and explored its neuroprotection role in intracerebral hemorrhage in vivo. Changes in inflammatory cytokines, such as TNF-α, IL-1ß and IL-6, reactive oxygen species (ROS) and NF-κB activation NF-κB were observed. In addition, the neurological deficit and cerebral water content of ICH mice were studied. The results demonstrated that sinomenine could inhibit the release of these cytokines and attenuate ROS production in a dose-dependent manner, and reduce NF-κB activation. Furthermore, sinomenine markedly inhibited cerebral water content and neurological deficit. In conclusion, our findings suggest that sinomenine played the protective effects through inhibition of microglial inflammation, and the findings also provided a novel therapy to treat ICH induced brain injury.

Microglial activation with reduction in autophagy limits white matter lesions and improves cognitive defects during cerebral hypoperfusion.

Microglial activation plays a vital role in the pathogenesis of white matter lesions (WMLs) during chronic cerebral hypo perfusion. Autophagy has been associated with both microglia survival and cell death. Yet, the role of autophagy during microglial activation in chronic cerebral ischemia is still unknown. We used a chronic cerebral hypoperfusion model by permanent stenosis of bilateral common carotid artery in mice to study microglial activation and autophagy. However, the autophagy inhibitor (3-methyladenine) could attenuate microglial autophagic activation, decrease white matter lesions, and improve working memory during chronic cerebral hypoperfusion in mice. In conclusion, chronic cerebral hypoperfusion that leads to microglial activation and autophagy induction exacerbates white matter lesions and cognitive deficits in mice. Our findings represent a potential novel target for chronic cerebral hypoperfusion therapy.

A novel nanoparticle containing MOG peptide with BTLA induces T cell tolerance and prevents multiple sclerosis.

Accumulative evidence demonstrates that multiple sclerosis (MS) is caused by activation of myelin Ag-reactive CD4+ T cells. Therefore, the CD4+ T cells specific for myelin Ag may be the important therapeutical target of MS. The novel coinhibitory receptor B and T lymphocyte attenuator (BTLA) may have a regulatory role in maintaining peripheral tolerance, however, its role in MS is still unknown. In this study, a novel nanoparticle containing MOG peptide with BTLA was designed and transduced into dendritic cells (DCs), and MOG peptide-induced EAE mice were administrated with the genetically modified DCs in vivo. The results demonstrated that modified DCs significantly enhanced the proportion of Foxp3+ CD4+ regulatory T cells, increased IL-10 and TGF-ß cytokine secretion, while decreased IL-2 and IFN-γ cytokine secretion. Furthermore, modified DCs supressed the CD4+ T cell response to MOG, cell infiltration into spinal cord, and the severity of EAE. In contrast, immune response to irrelevant exogenous Ag was not impaired by treatment with modified DCs. These findings suggested that DCs transduced with nanoparticle could induce specific CD4+ T-cells tolerance, which provided a promising therapeutic means to negatively manipulate immune response for autoimmune diseases without inhibition of the immune response to irrelevant Ag.

[Effects of simvastatin on expression of CTGF and α-SMA in renal tubulointerstitium of rats with diabetic nephropathy].

OBJECTIVE: To investigate the effects of low-dose simvastatin on the expression of connective tissue growth factor (CTGF) and α-smooth muscle actin (α-SMA) in the renal tubulointerstitium of rats with diabetic nephropathy. METHODS: Sixty male SD rats were randomly divided into three groups: Group C (control group), Group D, in which diabetes was induced by stroptozotocin (STZ) and Group DS, in which STZ-induced diabetic rats were treated with low-dose (no cholesterol-lowering effect) simvastatin. The following parameters were measured after 6 weeks and 12 weeks in each groups, respectively: body weight and kidney weight, 24-h urinary albumin excretion (UAE), biochemical indexes including blood glucose (GLU), low density lipoprotein (LDL), high density lipoprotein (HDL), triglycerides (TG) and serum creatinine (SCr). The expression of CTGF and α-SMA in renal tubulointerstitium was assessed by immunohistochemical method. RESULT: After 6 and 12 weeks, there were no significant differences in SCr, LDL, HDL and TG levels among all three groups. The expression levels of CTGF and α-SMA in the tubulointerstitium of Group DS were significantly decreased compared with those of Group D at week 6 (P<0.05); there were no significant differences compared with Group C (P>0.05). After 12 weeks, CTGF and α-SMA expressions in Group DS were also lower than those in Group D (P<0.05); while higher than those in Group C (P<0.05). CONCLUSION: Simvastatin with a under cholesterol-lowering dose, can decrease the expression levels of CTGF and α-SMA in renal tubulointerstitium of rats with diabetic nephropathy, by which the progression of the tubulointerstitial fibrosis would be delayed.

Clinical study of plasma thrombomodulin detection.

The purpose of this study was to investigate the clinical value of plasma thrombomodulin (PTM) in different diseases or in different severity or complications of diseases, PTM in 979 patients and 60 healthy controls was determined by ELISA method. The results showed that the PTM level in the control group was 20.40 +/- 7.72 microg/L, there was no difference in sex and ages. In chronic primary glomerular disease, the PTM level in chronic renal failure (CRF) group was higher than that in non-CRF group (P < 0.01). PTM level > 70 microg/L was defined as its positive criterion. The sensitivity, specificity and positive predictive value in PTM were 85.7%, 82.4% and 77.8% respectively. The PTM level in septemia group was higher than that in non-septemia group (P < 0.01), the sensitivity, specificity and positive predictive value were 86.6%, 89.5% and 76.5% respectively (> 50 microg/L as its positive criterion). With respect of multiple trauma, the PTM level in multiple organ failare (MOF) group was higher than that in non-MOF group (P < 0.01), while the sensitivity, specificity and positive predictive value were 77.8%, 77.3% and 73.7% respectively (> 40 microg/L as its positive criterion). For systemic lupus erythematosus (SLE), the PTM level in the patients with albuminuria was higher than that in the patients without albuminuria (P < 0.01), and the sensitivity, specificity and positive predictive value were 77.8%, 92.3% and 93.3% respectively (> 35.54 microg/L as its positive criterion). For diabetes, the PTM level in complication group was higher than that in group without complications, the sensitivity, specificity and positive predictive value were 53.4%, 97.1% and 98.6% respectively (> 35.54 microg/L as its positive criterion). The PTM level in microangiopathy group was higher than that in macroangiopathy group (P < 0.01). The sensitivity, specificity and positive predictive value were 71.2%, 97.1% and 97.9% respectively. Acute leukemia (AL) and multiple myeloma (MM) had higher PTM level and PTM level was extremely high when renal failure developed (P < 0.01). As compared the acute stage with the restoration stage in stroke, pre-chemotherapeutics with post-chemotherapeutics in AL and MM, and pre-operation with post-operation in cancer, the PTM level was connected with clinical development. The PTM level in the patients with microangiopathy was higher than that in the patients with macroangiopathy (P < 0.01). The defined PTM level was higher than its normal upper limit as PTM positive criterion in microangiopathy diseases, the sensitivity, specificity and positive predictive value were 77.7%, 71.2% and 75.6% respectively. It is concluded that PTM level is a good criterion in evaluating the microangiopathy, and PTM is also a valuable indicator in prediction or assessment of the severity of diseases, or evaluation of therapeutic effectiveness.

Effects of simvastatin on oxidative stress in streptozotocin-induced diabetic rats: a role for glomeruli protection.

AIMS: To study the effects of simvastatin on oxidative stress in rats with early stage diabetic nephropathy. METHODS: 60 male Sprague-Dawley rats were divided into three groups: control group (CN), streptozotocin (STZ)-induced diabetic rats group (DM) and STZ-induced diabetic rats group treated with simvastatin (DM+S). The following parameters were measured at weeks 6 and 12 in similar rats chosen randomly from each group: body and kidney weight, 24-hour urinary albumin excretion (UAE), biochemical indexes including blood glucose (GLU), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides (TG), serum creatinine (SCr), antioxidant enzymes including superoxide dismutase (SOD), glutathione S-transferase (GST), catalase (CAT) in plasma, lipid peroxidation production as malondialdehyde in plasma (MDAp) and erythrocytes (MDAe), morphology parameters such as glomerular volume (GV) and mesangial area/total glomerular area (M/T). RESULTS: At weeks 6 and 12, GLU and kidney weight to body weight ratio were notably increased in both of the diabetic groups compared with those in the CN group without significant differences between the two diabetic groups. There were no significant differences of SCr, LDL, HDL and TG among all groups within all the experimental time. MDAp and MDAe were significantly increased in both of the diabetic groups, especially at week 12, while SOD, GST and CAT were significantly decreased compared with those in the CN group. At week 12, GV, M/T and UAE were also increased in the two diabetic groups. However, in the DM+S group, changes of lipid peroxidation production, antioxidant enzymes, UAE and GV were less pronounced than those in the DM group. Pearson's correlation analysis and regression analysis shown that MDAp was increased while SOD, GST and CAT in plasma were decreased with elevation of UAE, GV and M/T. CONCLUSION: Increased lipid peroxidation and decreased antioxidant enzymes in plasma may play a role in the progression of diabetic nephropathy. Simvastatin may ameliorate these changes to protect kidney from oxidative lesion in diabetes even in the absence of lipid abnormalities.

Oxidative stress and damage induced by abnormal free radical reactions and IgA nephropathy.

OBJECTIVE: To estimate the oxidative stress and oxidative damage induced by abnormal free radical reactions in IgA nephropathy (IgAN) patients' bodies. METHODS: Seventy-two IgA N patients (IgANP) and 72 healthy adult volunteers (HAV) were enrolled in a random control study design, in which the levels of nitric oxide (NO) in plasma, lipoperoxide (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (beta-CAR) in plasma as well as the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric methods. RESULTS: Compared with the HAV group, the averages of NO in plasma, and LPO in plasma and in erythrocytes in the IgANP group were significantly increased (P<0.0001), while those of VC, VE and beta-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the IgANP group were significantly decreased (P<0.0001). Linear correlation analysis showed that with the increase of the values of NO, and LPO in plasma and in erythrocytes, and with the decrease of those of VC, VE, beta-CAR, SOD, CAT and GPX in the IgAN patients, the degree of histological damage of tubulointerstitial regions was increased gradually (P<0.0001); and that with the prolongation of the duration of disease the values of NO, and LPO in plasma and erythrocytes were increased gradually, while those of VC, VE, beta-CAR, SOD, CAT and GPX were decreased gradually (P<0.005). The discriminatory correct rates of the above biochemical parameters reflecting oxidative damage of the IgAN patients were 73.8%-92.5%, and the correct rates for the HAV were 70.0%-91.3% when independent discriminant analysis was used; and the correct rate for the IgAN patients was increased to 98.8%, the correct rate for the HAV was increased to 100% when stepwise discriminant analysis was used. The above biochemical parameters' reliability coefficient (alpha) were used to estimate the oxidative damage of the IgAN patients as 0.8145, the standardized item alpha=0.9730, F=53273.5681, P<0.0001. CONCLUSIONS: A series of free radical chain reactions caused serious pathological aggravation in the IgANP' bodies, thus resulting in oxidative damage in their bodies. In treating IgANP, therefore, it is necessary that suitable dose antioxidants should be supplemented to them so as to alleviate the oxidative damage in their bodies.

Abnormal reactions of free radicals and oxidative damages in the bodies of patients with chronic glomerulonephritis.

OBJECTIVE: To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis. METHODS: Eighty chronic glomerulonephritis patients (CGNP) and eighty healthy adult volunteers (HAV) were enrolled in a random control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (beta-CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric assays. RESULTS: Compared with the average values of the above biochemical parameters in the HAV group, the average values of NO in plasma, and LPO in plasma and erythrocytes in the CGNP group were significantly increased (P = 0.0001), while those of VC, VE and beta-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CGNP group were significantly decreased (P = 0.0001). Pearson product-moment correlation analysis showed that with increase of the concentration of blood creatinine as well as prolongation of the course of disease in the CGNP, the concentrations of NO in plasma, and LPO in plasma and erythrocytes in the CGNP increased gradually, while the concentrations of VC, VE and beta-CAR in plasma as well as the activities of SOD, CAT and GPX in erythrocytes in the CGNP decreased gradually (P = 0.002454-0.000001). The relative risk ratio (RR) of the above biochemical parameters reflecting oxidative damages in the bodies of CGNP ranged from 6.061 to 72.429. The reliability coefficient (alpha) that the above biochemical parameters were used to reflect the oxidative damages of the CGNP was 0.8137, standardized item alpha = 0.9728, Hotelling's T-Squared = 1135680.191, F = 53274.6478, P = 0.000001. CONCLUSIONS: The findings in this study show that in the bodies of CGNP a series of free radical chain reactions result in severe pathological aggravation and induce oxidative damages in their bodies. Therefore, suitable dose of antioxidants should be supplemented to them so as to alleviate oxidative damages in their bodies.