Abstract：
BACKGROUND: Cinnamic acid (Cinn) is a phenolic acid of Cinnamomum cassia (L.) J. Presl. that can ameliorate diabetic nephropathy (DN). However, comprehensive therapeutic targets and underlying mechanisms for Cinn against DN are limited.
OBJECTIVE: In this study, a network pharmacology approach and in vivo experiments were adopted to predict the pharmacological effects and mechanisms of Cinn in DN therapy.
METHODS: The nephroprotective effect of Cinn on DN was investigated by a streptozotocininduced diabetes mellitus (DM) mouse model. The protein-protein interaction network of Cinn against DN was established by a network pharmacology approach. The core targets were then identified and subjected to molecular docking with Cinn.
RESULTS: Cinn treatment effectively restored body weight, ameliorated hyperglycemia, and reduced kidney dysfunction markers in DM mice, also demonstrating a reduction in tissue injury. Network pharmacology analysis identified 298 DN-Cinn co-target genes involved in various biological processes and pathways. Seventeen core targets were identified, eight of which showed significant differential expression in the DN and healthy control groups. Molecular docking analysis revealed a strong interaction between Cinn and PTEN. Cinn treatment downregulated the PTEN protein expression in DM mice.
CONCLUSIONS: This study revealed the multi-target and multi-pathway characteristics of Cinn against DN. Cinn improved renal pathological damage of DN, which was related to the downregulation of PTEN.
OBJECTIVE: In this study, a network pharmacology approach and in vivo experiments were adopted to predict the pharmacological effects and mechanisms of Cinn in DN therapy.
METHODS: The nephroprotective effect of Cinn on DN was investigated by a streptozotocininduced diabetes mellitus (DM) mouse model. The protein-protein interaction network of Cinn against DN was established by a network pharmacology approach. The core targets were then identified and subjected to molecular docking with Cinn.
RESULTS: Cinn treatment effectively restored body weight, ameliorated hyperglycemia, and reduced kidney dysfunction markers in DM mice, also demonstrating a reduction in tissue injury. Network pharmacology analysis identified 298 DN-Cinn co-target genes involved in various biological processes and pathways. Seventeen core targets were identified, eight of which showed significant differential expression in the DN and healthy control groups. Molecular docking analysis revealed a strong interaction between Cinn and PTEN. Cinn treatment downregulated the PTEN protein expression in DM mice.
CONCLUSIONS: This study revealed the multi-target and multi-pathway characteristics of Cinn against DN. Cinn improved renal pathological damage of DN, which was related to the downregulation of PTEN.
摘要：
背景：肉桂酸（Cinn）是肉桂的酚酸（L.)J.Presl。可以改善糖尿病肾病（DN）。然而,Cinn抗DN的综合治疗靶点和潜在机制是有限的。
目的：在本研究中，采用网络药理学方法和体内实验来预测Cinn在DN治疗中的药理作用和机制。
方法：通过链脲佐菌素诱导的糖尿病（DM）小鼠模型研究了Cinn对DN的肾保护作用。通过网络药理学方法建立了Cinn抗DN的蛋白质-蛋白质相互作用网络。然后鉴定核心靶标并进行与Cinn的分子对接。
结果：Cinn治疗有效恢复了体重，改善高血糖，和减少DM小鼠的肾功能障碍标志物，也证明了组织损伤的减少。网络药理学分析确定了298个涉及各种生物过程和途径的DN-Cinn共靶基因。确定了十七个核心目标，其中8个在DN组和健康对照组中表现出显著差异表达。分子对接分析揭示了Cinn和PTEN之间的强相互作用。Cinn治疗下调DM小鼠的PTEN蛋白表达。
结论：本研究揭示了Cinn抗DN的多靶点、多途径特性。Cinn改善DN的肾脏病理损害，这与PTEN的下调有关。
目的：在本研究中，采用网络药理学方法和体内实验来预测Cinn在DN治疗中的药理作用和机制。
方法：通过链脲佐菌素诱导的糖尿病（DM）小鼠模型研究了Cinn对DN的肾保护作用。通过网络药理学方法建立了Cinn抗DN的蛋白质-蛋白质相互作用网络。然后鉴定核心靶标并进行与Cinn的分子对接。
结果：Cinn治疗有效恢复了体重，改善高血糖，和减少DM小鼠的肾功能障碍标志物，也证明了组织损伤的减少。网络药理学分析确定了298个涉及各种生物过程和途径的DN-Cinn共靶基因。确定了十七个核心目标，其中8个在DN组和健康对照组中表现出显著差异表达。分子对接分析揭示了Cinn和PTEN之间的强相互作用。Cinn治疗下调DM小鼠的PTEN蛋白表达。
结论：本研究揭示了Cinn抗DN的多靶点、多途径特性。Cinn改善DN的肾脏病理损害，这与PTEN的下调有关。
