Toll-like Receptor 4 Signaling Pathway in the Protective Effect of Pioglitazone on Experimental Immunoglobulin A Nephropathy / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>In vitro experiments have revealed that toll-like receptor 4 (TLR4) pathway is involved in the progression of immunoglobulin A nephropathy (IgAN) by induction of proinflammatory cytokines. Evidence showed that, in other disease models, peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists have been shown to exert anti-inflammatory effects through suppression of the expression and activity of TLR4. However, the interaction between PPAR-γ and TLR4 in IgAN has not been fully studied both in vitro and in vivo. In this study, we explored whether TLR4 pathway attributed to the progression of IgAN in experimental rats.</p><p><b>METHODS</b>Bovine gamma globulin was used to establish IgAN model. Fifty-four Lewis rats were randomly divided into six groups: ControlTAK242, IgANTAK242, toll-like receptor 4 inhibitor (TAK242) groups (rats were administrated with TLR4 inhibitor, TAK242) and ControlPio, IgANPio, Pio groups (rats were administrated with PPAR-γ agonist, pioglitazone). Urinary albumin-to-creatinine ratio (ACR), serum creatinine, and blood urea nitrogen were detected by automatic biochemical analyzer. Renal histopathological changes were observed after hematoxylin-eosin staining, and the IgA deposition in glomeruli was measured by immunofluorescence staining. Real-time polymerase chain reaction and Western blotting were used to detect TLR4 and interleukin-1 beta (IL-1β) message ribonucleic acid (mRNA) and protein expression in renal tissues. Results were presented as mean ± standard deviation. Differences between groups were analyzed by one-way analysis of variance.</p><p><b>RESULTS</b>Compared to normal rats, experimental rats showed higher ACR (4.45 ± 1.33 mg/mmol vs. 2.89 ± 0.96 mg/mmol, P < 0.05), obvious IgA deposition with mesangial hypercellularity, hyperplasia of mesangial matrix accompanied by increased serum IL-1β (48.28 ± 13.49 pg/ml vs. 35.56 ± 7.41pg/ml, P < 0.05), and renal expression of IL-1β and TLR4. The biochemical parameters and renal pathological injury were relieved in both TAK242 group and Pio group. The expressions of renal tissue TLR4, IL-1β, and serum IL-1β were decreased in rats treated with TAK242, and the expression of TLR4 mRNA and protein was significantly reduced in Pio group compared to IgANPiogroup (1.22 ± 0.28 vs. 1.72 ± 0.45, P < 0.01, and 0.12 ± 0.03 vs. 0.21 ± 0.05, P < 0.01).</p><p><b>CONCLUSIONS</b>Our study proves that inflammation mediated by TLR4 signaling pathway is involved in the progression of IgAN in rat models. Moreover, pioglitazone can inhibit the expression of TLR4 in IgAN.</p>

Anatomical study of the third palmar interosseous muscle and its dominate nerve / 中华显微外科杂志

Objective To explore the anatomical characteristic of the third palmar interosseous mus- cle as well its dominate nerve,and to investigate the anatomical basis of difficult recovery of digitus minimus adduction.Methods Twenty aduh fresh hands without deformity and trauma were obtained.Dissect and observe the third palmar interosseous muscle and its dominate nerve and adjacent structure under surgical mi- croseope,measure the size of the third pahnar interosseous muscle and its dominate nerve,the data were pro- cessed by stastistics method.Results Among palmar interosseous muscles and its dominate nerves,the third palmar interosseous muscle and its dominate nerve is the smallest.There are conspicuous tendon bundle on the surface of the third palmar interosseous muscle partly,which have a potential compression on the third palmar interosseous muscle dominting nerve.Conclusion The third palmar interosseous muscle is the smal- lest among palmar interusseous muscles and it is the only digitus minimus adduction muscle.The sominating nerve of the third palmar interosseous muscle is small anti the tendon bundle of the third palmar interosseous muscle have a potential compression.All these can cast light on diffcult recovery of digitus minimus adduction.