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Immune-related nephropathy (IRN) refers to immune-response-mediated glomerulonephritis and is the main cause of end-stage renal failure. The pathogenesis of IRN is not fully understood; therefore, treatment is challenging. Traditional Chinese medicines (TCMs) have potent clinical effects in the treatment of the IRN conditions immunoglobulin A nephropathy, lupus nephropathy, and diabetic nephropathy. The underlying mechanisms mainly include its inhibition of inflammation; improvements to renal interstitial fibrosis, oxidative stress, autophagy, apoptosis; and regulation of immunity. In this review, we summarize the clinical symptoms of the three IRN subtypes and the use of TCM prescriptions, herbs, and bioactive compounds in treating IRN, as well as the potential mechanisms, intending to provide a reference for the future study of TCM as IRN treatments.

Study on anti-fatigue, anti-oxidative and hemostatic effects of small molecule Asini Corii Colla / 中国药理学通报

Aim: To study the anti-fatigue,anti-oxidative and hemostatic effects of small molecule Asini Corii Colla (SMACC). Methods: Rat model of complex blood deficiency was established to detect the exhausted time of swimming, hematology, superoxide dismutase (SOD), serum maleic dialdehyde (MDA), and lipid peroxide (LPO) levels, aiming to explore the anti-fatigue and anti-oxidative effects of SMACC. ICR mice were used to measure the blood clotting time (CT) and bleeding time (BT). Fevered and bleeding model and the heparinized bleeding model in rats were established to investigate the effect of SMACC in hemostasis and its possible mechanism. Results: Compared with model group, SMACC significantly prolonged the swimming time of model rats (P < 0. 05, P < 0. 01) and decreased the content of serum MDA, LPO (P < 0.05,P<0.01) at doses of 1. 500,0. 750,0. 375 g. kg-1,and increased the number of lymphocytes in the blood at doses of 1. 500,0. 375 g. kg-1 (P <0. 05). SMACC of 3. 00,1.50 g kg-1 significantly reduced the BT and CT (P < 0. 05). SMACC markedly reversed the prolonged prothrombin time (P < 0. 05) and the adverse changes of the hematological indicators. Conclusions: SMACC has the pharmacological effects of anti-fatigue, anti-oxidation and enhancing endurance, and also the effects of hemostasis and convergence.

Effect of γ-secretase inhibitor on hyperoxia-induced brain white matter injury in mice / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of γ-secretase inhibitor (N-[N-(3,5-difluorophenacetyl)-l -alanyl]-S-phenylglycine t-butyl ester, DAPT) on hyperoxia-induced brain white matter injury in mice.</p><p><b>MWTHODS</b>Three-day-old C57BL/10J mouse pups were divided into air control (C) group, control+DAPT (10 mg/kg, injected intraperitoneally) group, hyperoxia group (exposed to 80% oxygen for 48 h), and hyperoxia+DAPT group. The brain and body weights of the mice were measured at postnatal days 3, 5, 12, and 28. Real-time PCR was used to detect Notch intracellular domain (NICD) mRNA expression in the brain after modeling, and the expressions of NG2 and myelin basic protein (MBP) were detected by double-labeled immunofluorescence assay to verify the oligdendrocycle type at postnatal day 12. The mice in each group were bred until postnatal day 28 for Morris water maze test.</p><p><b>RESULTS</b>The brain and body weights were significantly decreased in mice in hyperoxia group compared to the control mice, but increased significantly after DAPT treatment (P<0.05). Real-time PCR showed that a 48-hour hyperoxia exposure significantly increased NICD mRNA expression in the brain (P<0.05), which was decreased by co-treatment by DAPT (P<0.05). Hyperoxia also resulted in enhanced NG2 expression and lowered MBP expression in the brain (P<0.05). Compared with the control mice, the mice exposed to hyperoxia showed prolonged escape latency (P<0.05) and spent less time in the target quadrant with a lowered number of passing through the virtual platform (P<0.05). All these parameters were significantly improved by co-treatment with DAPT.</p><p><b>CONCLUSION</b>Specific inhibition of Notch signaling pathway activation in the brain by the γ-secretase inhibitor DAPT can ameliorate white matter injury and learning and memory impairment in newborn mice with hyperoxia exposure.</p>

Lipopolysaccharide sensitizes neonatal mice to hyperoxia-induced immature brain injury / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the effect of low-concentration lipopolysaccharide (LPS) pretreatment on hyperoxia-induced immature brain injury in neonatal mice and explore and the related mechanisms.</p><p><b>METHODS</b>Forty-eight neonatal mice on postnatal day 3 (PND3) were randomized into normal control group, LPS (0.3 mg/kg) group, hyperoxia group (hyperoxia exposure for 24 h), and hyperoxia+LPS group (hyperoxia exposure for 24 h 30 min after 0.3 mg/kg LPS treatment). At PND5, all the neonatal mice were sacrificed to examine the morphological changes of microglia in the periventricular white matter using Tomato lectin staining, measure malondialdehyde (MDA) content in the immature brain, detect mRNA expression of tumor necrosis factor-α (TNF-α) using real-time PCR, and determine caspase-3 protein expression with Western blotting.</p><p><b>RESULTS</b>Compared with the control group, exposures to LPS, hyperoxia, and both all resulted in microglia activation in the periventricular white matter. The number of activated microglia, MDA content, TNF-α mRNA expression and caspase-3 protein expression in the immature brain were significantly higher in hyperoxia group than in the control group and LPS group (P<0.05). LPS pretreatment significantly enhanced hyperoxia-induced microglia activation in the immature brain (P<0.05).</p><p><b>CONCLUSION</b>Hyperoxia causes immature brain injury mediated by microglia activation, and LPS pretreatment can enhance such brain injury in neonatal mice.</p>

Effect of hyperoxia exposure on the function of N9 microglia in vitro / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effect of normobaric hyperoxia exposure on the functions of N9 microglia and explore the underlying mechanism of hyperoxia-induced immature brain injury.</p><p><b>METHODS</b>N9 microglial cells were exposed to 900 ml/L O(2) for 2, 6, 12, 24 or 48 h, and the cell apoptotic rate was assessed using flow cytometry. The intracellular oxidative stress was measured using a fluorescent DCFH-DA probe, and the expression of Toll-like receptor 4 (TLR4) mRNA was detected using RT-PCR. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) concentrations in the supernatant of the cell cultures were tested with ELISA following the exposures. TLR4 protein expression was observed using immunofluorescence staining.</p><p><b>RESULTS</b>Significant cell apoptosis was detected after oxygen exposures for 12-24 h. Accumulation of reactive oxygen species (ROS) were detected after a 2-h exposure. After prolonged hyperoxia exposure, TLR4 expression and IL-1β and TNF-α levels significantly increased in the cells.</p><p><b>CONCLUSION</b>Hyperoxia exposure activates TLR4 signaling pathway in N9 microglial cells in vitro, leading to massive production of ROS, IL-1β, and TNF-α and thus triggering cell apoptosis.</p>

Expression of thyroid transcription factor-1 and vimentin in neonatal mice with bronchopulmonary dysplasia / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the expressions of thyroid transcription factor-1 (TTF-1), the type II alveolar epithelial cells (AECII)-specific marker, and vimentin, the fibroblast-specific marker, in the lungs of neonatal mice with bronchopulmonary dysplasia (BPD) and explore the pathogenesis of BPD.</p><p><b>METHODS</b>Neonatal mice were exposed to hyperoxia to induce BPD, and pathological changes in the lung tissues were examined. At 3, 7, 14 and 21 days after the exposure, the protein and mRNA expressions of TTF-1 and vimentin were detected by double-labeled immunofluorescence assay and real-time PCR, respectively.</p><p><b>RESULTS</b>Compared with the neonatal mice exposed in normal air, those with hyperoxic exposure showed developmental disorders and collagen deposition in the lung tissues. The protein expression of TTF-1 decreased while vimentin expression increased in the lung tissues, where their co-expression was observed at 14 and 21 days after the exposure. TTF-1 mRNA expression decreased markedly (P<0.05) and vimentin mRNA increased significantly in the lung tissues at 21 days after hyperoxic exposure of the mice (P<0.05).</p><p><b>CONCLUSION</b>Hyperoxia-induced transition of AECII to fibroblasts may play an important role in pulmonary fibrosis in neonatal mice with BPD.</p>

Effects of mechanical ventilation and controlled spontaneous respiration on pulmonary function during short duration of general anesthesia with tracheal intubation / 南方医科大学学报

<p><b>OBJECTIVE</b>To evaluate the effects of mechanical ventilation on pulmonary function during short duration of general anesthesia with tracheal intubation, and assess the safety of controlled spontaneous respiration during general anesthesia.</p><p><b>METHODS</b>Fifty-three adult patients (aged 18-55 years, ASA physical status I-II) scheduled for elective unilateral tympanoplasty were randomly assigned into mechanical ventilation group (group M, n=28) and spontaneous respiration group (group S, n=25). Anesthesia induction was performed in group M with intravenous propofol (2 mg/kg), fentanyl (3 microg<kg) and vecuronium (0.1 mg<kg), while with propofol (2 mg/kg), fentanyl (3 microg/kg) and sufficient superficial anesthesia on upper airway mucous membrane in group S. After tracheal intubation, mechanical ventilation began with VT 8 ml<kg and RR 10-12 bpm in group M, and spontaneous respiration was maintained in group S. Anesthesia was maintained by 0.7%-0.8% isoflurane and 60%-70% N(2)O at the end respiratory concentration to control MAC between 1.2-1.3. During the surgery, BIS values were controlled between 40-60, and propofol was administered when necessary. Vecuronium (1-2 mg) was given intermittently to maintain muscle relaxation and neostigmine (1 mg) with atropine 0.5 mg was administered intravenously before extubation in group M. No relaxant was used in group S. The parameters including heart rate (HR), mean blood pressure (MAP), pulse oxygen saturation (SpO(2)), and thoracic fluid content (TFC) were recorded before the induction and at 1, 5, 10, 20, 40, 60, 90, 120, and 150 min after intubation. Arterial blood was drawn immediately and 150 min after intubation for blood gases analysis and Alveolar-arterial oxygen gradient (P(A-a)DO(2)), and the respiratory index (RI) and dead volume/tidal volume (VD/VT) were calculated. The incidences of moving, bucking, swallowing, and status of awareness during surgery procedures were also recorded.</p><p><b>RESULTS</b>A total of 43 patients (group M, n=23; group S, n=20) were included in the study with 10 dropouts due to failed attempt to obtain arterial blood samples (8 patients) or severe bucking during intubation (2 patients). No significant differences were found in HR and MAP between the two groups (P>0.05). The pH and SpO(2) [ (97.9-/+1.00)% at the lowest] and PaO(2) in group S were significantly lower and the PaCO(2) was higher than those in group M (P<0.05). In group S, the pH values were 7.274-/+0.025 and 7.331-/+0.039, PaCO(2) values were 60-/+6 and 53-/+5 mmHg, and PETCO(2) values were 53-/+ 6 and 48-/+7 mmHg, and the PaO(2) values were 143-/+37 and 165-/+49 mmHg immediately and 150 min after the intubation, respectively. These values were considered safe under the concept of permissive hypercapnia. No significant differences were found in the P(A-a)DO(2), RI, VD/VT and TFC between or within the two groups (P>0.05), nor were moving, bucking, swallowing and awareness recorded during the surgical procedures.</p><p><b>CONCLUSION</b>In essentially normal lungs, short-term mechanical ventilation during general anesthesia with tracheal intubation does not damage the lung functions, and spontaneous respiration can offer sufficient oxygen supply without causing harmful carbon dioxide retention.</p>