Department of Pharmacy, Jaypee University of Information Technology, Waknaghat, Himachal Pradesh, 173234, India.
Dr. B.R. Ambedkar Center for Biomedical Research (ACBR), University of Delhi, North Campus, Delhi, 110 007, India.
Metab Brain Dis. 2018 Aug;33(4):1281-1292. doi: 10.1007/s11011-018-0243-1. Epub 2018 Apr 27.
The present study was aimed to investigate the effect of Urtica dioica Linn. (UD) extract against chronic diabetes mediated anxiogenic and depressive like behavior in mice. Streptozotocin (STZ) (50 mg/kg, i.p.) for 5 consecutive days was used to induce diabetes followed by treatment with UD leaves extract (50 mg/kg, p.o.) and rosiglitazone (ROSI) (5 mg/kg, p.o.) for 8 weeks. STZ induced chronic diabetes significantly induced anxiety and depressive like behavior in mice. Chronic diabetes significantly downregulated BDNF (p < 0.001), TrKB (p < 0.001), Cyclin D1 (p < 0.001), Bcl2 (p < 0.05) and autophagy7 (p < 0.001), while upregulated iNOS (p < 0.05) mRNA expression in the hippocampus as compared to control mice. In addition, chronic diabetes significantly increased the expression of TNF-α in CA1 (p < 0.001), CA2 (p < 0.01), CA3 (p < 0.001) and DG (p < 0.001) regions of hippocampus as compared to control mice. Chronic diabetes mediated neuronal damage in the CA2, CA3 and DG regions of hippocampus. Chronic administration of UD leaves extract significantly reversed diabetes mediated anxiogenic and depressive like behavior in mice. Further, UD treatment significantly upregulated BDNF (p < 0.01), TrKB (p < 0.001), Cyclin D1 (p < 0.001), Bcl2 (p < 0.01), autophagy5 (p < 0.01) and autophagy7 (p < 0.001), while downregulated iNOS (p < 0.05) mRNA expression in the hippocampus of diabetic mice. Concomitantly, UD administration significantly decreased the expression of TNF-α in hippocampal CA1 (p < 0.001), CA2 (p < 0.01), CA3 (p < 0.001) and DG (p < 0.001) regions of diabetic mice. Diabetes mediated neuronal damage and DNA fragmentation in the hippocampus was substantially attenuated following UD treatment. UD leaves extract might prove to be effective for diabetes mediated anxiety and depressive like behavior.
本研究旨在探讨荨麻（Urtica dioica Linn.）提取物对慢性糖尿病介导的焦虑和抑郁样行为的影响。连续 5 天腹腔注射链脲佐菌素（STZ）（50mg/kg）诱导糖尿病，随后用荨麻叶提取物（50mg/kg，po）和罗格列酮（ROSI）（5mg/kg，po）治疗 8 周。STZ 诱导的慢性糖尿病显著诱导了小鼠的焦虑和抑郁样行为。慢性糖尿病显著下调了 BDNF（p<0.001）、TrKB（p<0.001）、Cyclin D1（p<0.001）、Bcl2（p<0.05）和自噬 7（p<0.001）的 mRNA 表达，同时增加了海马 CA1 区 iNOS（p<0.05）的 mRNA 表达。此外，与对照组相比，慢性糖尿病显著增加了海马 CA1（p<0.001）、CA2（p<0.01）、CA3（p<0.001）和 DG（p<0.001）区 TNF-α的表达。慢性糖尿病介导了海马 CA2、CA3 和 DG 区神经元损伤。慢性给予荨麻叶提取物显著逆转了糖尿病介导的小鼠焦虑和抑郁样行为。此外，荨麻治疗显著上调了 BDNF（p<0.01）、TrKB（p<0.001）、Cyclin D1（p<0.001）、Bcl2（p<0.01）、自噬 5（p<0.01）和自噬 7（p<0.001）的 mRNA 表达，同时下调了糖尿病小鼠海马中 iNOS（p<0.05）的 mRNA 表达。同时，荨麻给药显著降低了糖尿病小鼠海马 CA1（p<0.001）、CA2（p<0.01）、CA3（p<0.001）和 DG（p<0.001）区 TNF-α的表达。糖尿病介导的海马神经元损伤和 DNA 片段化在荨麻治疗后明显减轻。荨麻叶提取物可能对糖尿病介导的焦虑和抑郁样行为有效。
