| 邱敏,陈波.组织蛋白酶 L对糖尿病大鼠肾脏炎症及氧化应激指标的影响[J].安徽医药,2021,25(6):1099-1103. |
| 组织蛋白酶 L对糖尿病大鼠肾脏炎症及氧化应激指标的影响 |
| Effect of cathepsin L on inflammation and oxidative stress of the kidneys in diabetic rats |
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| DOI：10.3969/j.issn.1009-6469.2021.06.009 |
| 中文关键词: 组织蛋白酶 L 糖尿病肾病 白细胞介素 -1 白细胞介素 -6 肿瘤坏死因子 α 丙二醛 超氧化物歧化酶 谷胱甘肽过氧化酶 大鼠， Sprague-Dawley |
| 英文关键词: Cathepsin L Diabetic nephropathies Interleukin-1 Interleukin-6 Tumor necrosis factor-alpha Malondialdehyde Superoxide dismutase Glutathione peroxidase Rats, Sprague-Dawley |
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| 中文摘要: |
| 目的观察组织蛋白酶 L(Cat L)对糖尿病大鼠肾脏炎症及氧化应激指标的影响，探索 Cat L在糖尿病肾病发生发展中的作用。方法将 30只 SD雄性大鼠采用随机数字表法分为对照组和糖尿病组，分别为 10只和 20只。腹腔注射链脲佐菌素建立糖尿病大鼠模型，建立成功后从糖尿病组取 10只大鼠每天腹腔注射 10 mg/kg Cat L抑制剂 Z-FY-CHO，作为抑制剂组。之后 4周、 8周分别收集三组各 5只大鼠 24 h尿，采血并处死大鼠取肾组织。全自动生化分析仪检测各组大鼠的尿蛋白、血尿素氮和血肌酐含量，实时荧光定量逆转录聚合酶链反应(qRT-PCR)检测 Cat L的 mRNA表达，试剂盒测定 Cat L活性、白细胞介素 1(IL-1)、白细胞介素 -6(IL-6)、肿瘤坏死因子 α(TNF-α)、丙二醛、超氧化物歧化酶( SOD)、谷胱甘肽过氧化酶( GSH-Px)和谷胱甘肽水平并比较。结果与对照组相比，糖尿病大鼠血糖持续较高、体质量减轻，而肾脏组织中 Cat L mRNA表达增加［4周(0.79±0.06)比( 1.02±0.14)， 8周( 0.54±0.10)比( 0.93±0.19)］，且活性增强［4周( 218.90±23.35)%比( 404.00±94.46)%，8周(283.10±29.99)%比( 463.80±85.32)%］。与正常大鼠比，糖尿病大鼠尿蛋白增加［8周( 52.06±7.75)mg/24 h］、血尿素氮［8周(342.2±54.9)mg/L］和血肌酐［8周( 282±68)μmol/L］水平升高；与糖尿病组相比， Cat L拮抗剂处理组大鼠尿蛋白减少［8周(38.12±5.98)mg/24 h］、血尿素氮［8周( 228.4±32.3)mg/L］和血肌酐［8周( 157±51)μmol/L］水平降低。与正常大鼠比，糖尿病大鼠肾组织中炎性因子 IL-1［8周( 58.94±27.52)ng/L］、 IL-6［8周( 39.25±3.47)ng/L］和 TNF-α［8周( 257.73±78.88)ng/L］水平增加、氧化应激相关指标丙二醛表达增加［8周( 0.97±0.14)nmol/mg］，SOD、GSH-Px和谷胱甘肽水平降低［8周( 25.86±3.62)U/mg、8周(13.03±1.76)U/mg、8周(3.00±0.61)μmol/g］而 Cat L拮抗剂抑制了这一改变［8周 IL-1(27.84±2.81)ng/L、IL-6(33.41±4.72)ng/L、 TNF-α(150.78±56.07)ng/L、丙二醛( 0.52±08)nmol/mg、SOD(36.55±4.35)U/mg、GSH-Px(18.54±2.26)U/mg、谷胱甘肽( 5.93±11.65)μmol/g］。结论 Cat L促进糖尿病大鼠肾脏炎症反应和氧化应激的发生，抑制 Cat L可减轻糖尿病肾损伤。 |
| 英文摘要: |
| Objective To clarify the effect of cathepsin L (Cat L) on kidney inflammation and oxidative stress in diabetic rats, and tostudy the role of Cat L in the development of diabetic nephropathy.Methods Thirty SD male rats were assigned into normal control group (n=10) and diabetes group (n=20) according to random number table method. The diabetic rat model was established by an intraperitoneal injection of streptozotocin. Then 10 rats of the diabetes group received an intraperitoneal injection of 10 mg/kg Cat L inhibitor Z-FY-CHO, taken as inhibitor group. At 4 and 8 weeks after diabetes induction, 24 h urine and blood of 5 respective rats from thethree groups was collected before the rats were sacrificed to obtain kidney tissues. Automatic biochemical analyzer was used to detectthe levels of urine protein, serum urea nitrogen (BUN) and creatinine (Cr) of rats in each group. Cat L mRNA expression was measuredby real-time fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR), Cat L activity, the levels of interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and GSH were detected and compared by kits.Results Compared with the control group, diabetic rats had sustained higher blood glucose, decreased body mass, increased Cat L mRNA expression [4W (0.79±0.06) vs. (1.02±0.14), 8W (0.54±0.10) vs. (0.93±0.19)] and increased activity [4W (218.90±23.35) % vs. (404.00±94.46) %,8W (283.10±29.99) % vs. (463.80±85.32) %] inkidney tissues. Compared with normal rats, diabetic rats exhibited increased urine protein [8W (52.06±7.75) mg/24 h] and elevated serum BUN [8W (342.2±54.9) mg/L] and Cr [8W (282±68) μmol/L] levels. Compared with the diabetic group, the Cat L antagonist-treated group had lower urine protein [8W (38.12±5.98) mg/24h], serum BUN [8W (228.4±32.3) mg/L] and Cr [8W (157±51) μmol/L] levels.Compared with normal rats, the levels of inflammatory factors IL-1 [8W (58.94±27.52) ng/L], IL-6 [8W (39.25±3.47) ng/L] and TNF-α [8W (257.73±78.88) ng/L] increased in the kidney tissues of diabetic rats, and the level of oxidative stress-related indicators such as MDA increased [8W (0.97±0.14) nmol/mg], while SOD, GSH-Px and GSH decreased [8W (25.86±3.62) U/mg, 8W (13.03±1.76) U/mg,8W (3.00±0.61) μmol/g]. Cat L antagonist inhibited the changes [8W IL-1: (27.84±2.81) ng/L, IL-6: (33.41±4.72) ng/L, TNF-α: (150.78±56.07) ng/L, MDA: (0.52±0.18) nmol/mg, SOD: (36.55±4.35) U/mg, GSH-Px: (18.54±2.26) U/mg, GSH: (5.93±1.65) μmol/g] Conclusion Cat L can promote the inflammatory response and oxidative stress in the diabetic kidney of rats, and inhibition of Cat Lcan reduce kidney injury in diabetic rats. |
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