蛇床子素调节Mincle/Syk/NF-κB信号通路对肾病综合征大鼠的治疗作用

doi:10.3969/j.issn.1006-6233.2023.03.06

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Abstract Objective: To investigate the therapeutic effect of osthol (OST) on nephrotic syndrome (NS) in rats by regulating macrophage-inducible C-type lectin (Mincle)/spleen tyrosine kinase (Syk)/nuclear factor-κB (NF-κB) signal pathway. Methods: Ten rats were randomly selected and recorded as group N, and other rats were used to construct NS model. The 50 successfully modeled rats were randomly divided into NS group (model group), L-OST group (10 mg/kg OST), M-OST group (20 mg/kg OST), H-OST group (40 mg/kg OST), H-OST+TDB group (40 mg/kg OST+50 μg TDB/week). OST was injected once a day for 4 consecutive weeks. The levels of inflammatory factors (IL-1β, IL-6, TNF-α), oxidative stress indicators (SOD, MDA, LDH) in serum and UP in 24h urine were detected by ELISA; the levels of BUN and Scr was measured by automatic chemical analyzer; HE staining and Masson staining were used to detect the pathological changes of kidney; TUNEL staining was used to detect renal cell apoptosis; Western blot was used to detect the expression of collagen I, Ly6g, Ki-67, and Mincle/Syk/NF-κB pathway proteins. Results: In group N, the renal tissue structure was normal and the staining was clear. In NS group, a large number of interstitial inflammatory cells infiltrated, renal tubules atrophied, and a large number of vacuoles were observed, compared with group N, the contents of 24h UP, Scr, BUN, levels of IL-1β, IL-6, TNF-α, MDA, LDH, the collagen volume fraction, apoptosis rate, the levels of collagen I, Ly6g, Ki-67, Mincle, Syk, p-NF-κB/NF-κB proteins in NS group increased significantly (P<0.05), the level of SOD decreased significantly (P<0.05); compared with NS group, the inflammatory cell infiltration and renal tubule atrophy in the L-OST group, M-OST group and H-OST group were improved, the contents of 24h UP, Scr, BUN, levels of IL-1β, IL-6, TNF-α, MDA, LDH, the collagen volume fraction, apoptosis rate, the levels of collagen I, Ly6g, Ki-67, Mincle, Syk, p-NF-κB/NF-κB proteins decreased significantly (P<0.05), the level of SOD increased significantly (P<0.05), the treatment effect of H-OST group was the best; TDB eliminated the ameliorative effect of OST on renal injury in NS rats. Conclusion: OST may alleviate renal injury in OST rats by inhibiting the Mincle/Syk/NF-κB signal pathway.

Key words： Osthol Nephrotic syndrome Mincle Syk NF-κB

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2023.03.06 OR http://www.hbyxzzs.cn/EN/Y2023/V29/I3/380

[1] Wang CS,Greenbaum LA.Nephrotic syndrome[J].Pediatr Clin North Am,2019,66(1):73-85.
[2] Downie ML,Gallibois C,Parekh RS,et al.Nephrotic syndrome in infants and children:pathophysiology and management[J].Paediatr Int Child Health,2017,37(4):248-258.
[3] Yu C,Li P,Qi D,et al.Osthole protects sepsis-induced acute kidney injury via down-regulating NF-κB signal pathway[J].Oncotarget,2017,8(3):4796-4813.
[4] Lv LL,Tang PM,Li CJ,et al.The pattern recognition receptor,Mincle,is essential for maintaining the M1 macrophage phenotype in acute renal inflammation[J].Kidney Int,2017,91(3):587-602.
[5] Tan RZ,Wang C,Deng C,et al.Quercetin protects against cisplatin-induced acute kidney injury by inhibiting Mincle/Syk/NF-κB signaling maintained macrophage inflammation[J].Phytother Res,2020,34(1):139-152.
[6] 王新斌,戴恩来,薛国忠,等.基于RhoA/ROCK通路探讨淫羊藿苷对肾病综合征大鼠的保护机制[J].中国实验方剂学杂志,2020,26(11):78-84.
[7] Yao H,Cai ZY,Sheng ZX.NAC attenuates adriamycin-induced nephrotic syndrome in rats through regulating TLR4 signaling pathway[J].Eur Rev Med Pharmacol Sci,2017,21(8):1938-1943.
[8] Garcia-Arroyo FE,Gonzaga-Sánchez G,Tapia E,et al. Osthol ameliorates kidney damage and metabolic syndrome induced by a high-fat/high-sugar diet[J].Int Mol Sci,2021,22(5):2431-2447.
[9] Huang T,Dong Z.Osthole protects against inflammation in a rat model of chronic kidney failure via suppression of nuclear factor-κB,transforming growth factor-β1 and activation of phosphoinositide 3-kinase/protein kinase B/nuclear factor (erythroid-derived 2)-like 2 signaling[J].Mol Med Rep,2017,16(4):4915-4921.
[10] Lu C,Zheng SF,Liu J.Forsythiaside A alleviates renal damage in adriamycin-induced nephropathy[J].Front Biosci (Landmark Ed),2020,25(3):526-535.
[11] Dong Y,Zhang Q,Wen J,et al.Ischemic duration and frequency determines AKI-to-CKD progression monitored by dynamic changes of tubular biomarkers in IRI mice[J].Front Physiol,2019,10(1):153-167.