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Anti-Inflammatory Effects and Molecular Mechanisms of Shenmai Injection in Treating Acute Pancreatitis: Network Pharmacology Analysis and Experimental Verification
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2022-08-02 , DOI: 10.2147/dddt.s364352 Yanqiu He 1 , Cheng Hu 1 , Shiyu Liu 1 , Mingjie Xu 1 , Ge Liang 2 , Dan Du 3 , Tingting Liu 1 , Fei Cai 1 , Zhiyao Chen 1 , Qingyuan Tan 1 , Lihui Deng 1 , Qing Xia 1
Drug Design, Development and Therapy ( IF 4.8 ) Pub Date : 2022-08-02 , DOI: 10.2147/dddt.s364352 Yanqiu He 1 , Cheng Hu 1 , Shiyu Liu 1 , Mingjie Xu 1 , Ge Liang 2 , Dan Du 3 , Tingting Liu 1 , Fei Cai 1 , Zhiyao Chen 1 , Qingyuan Tan 1 , Lihui Deng 1 , Qing Xia 1
Affiliation
Background: Acute pancreatitis (AP) is an inflammatory disorder of the exocrine pancreas without specific treatment. Shenmai injection (SMI) was reported to eliminate the severity of experimental AP. This study aimed to explore the mechanisms underlying the synergistic protective effects of SMI on AP based on network pharmacology and experimental validation.
Methods: Network pharmacology analysis and molecular docking based on identified components were performed to construct the potential therapeutic targets and pathways. The principal components of SMI were detected via ultra-high-performance liquid chromatography-coupled with quadrupole time-of-flight mass spectrometry (UHPLC-QTOF/MS). Effect of SMI and the identified components on cellular injury and IL6/STAT3 signaling was assessed on mouse pancreatic acinar cell line 266– 6 cells. Finally, 4% sodium taurocholate (NaT) was used to induce AP model to assess the effects of SMI in treating AP and validate the potential molecular mechanisms.
Results: By searching the TCMSP and ETCM databases, 119 candidate components of SMI were obtained. UHPLC-QTOF/MS analysis successfully determined the representative components of SMI: ginsenoside Rb1, ginsenoside Rg1, ginsenoside Re, and ophiopogonin D. Fifteen hub targets and eight related pathways were obtained to establish the main pharmacology network. Subnetwork analysis and molecular docking indicated that the effects of these four main SMI components were mostly related to the interleukin (IL) 6/STAT3 pathway. In vitro, SMI, ginsenoside Rb1, ginsenoside Rg1, ginsenoside Re, and ophiopogonin D increased the cell viability of NaT-stimulated mouse pancreatic acinar 266– 6 cells and decreased IL6 and STAT3 expression. In vivo, 10 mL/kg SMI significantly alleviated the pancreatic histopathological changes and the expression of IL6 and STAT3 in the AP mice.
Conclusion: This study demonstrated SMI may exert anti-inflammatory effects against AP by suppressing IL6/STAT3 activation, thus providing a basis for its potential use in clinical practice and further study in treating AP.
中文翻译：
参麦注射液治疗急性胰腺炎的抗炎作用及分子机制：网络药理分析与实验验证
背景：急性胰腺炎（AP）是一种未经特殊治疗的胰腺外分泌炎症性疾病。据报道参麦注射液 (SMI) 可消除实验性 AP 的严重性。本研究旨在基于网络药理学和实验验证，探索 SMI 对 AP 的协同保护作用的机制。
方法：进行基于已识别成分的网络药理学分析和分子对接，以构建潜在的治疗靶点和途径。通过超高效液相色谱-四极杆飞行时间质谱联用 (UHPLC-QTOF/MS) 检测 SMI 的主要成分。在小鼠胰腺腺泡细胞系 266-6 细胞上评估 SMI 和已识别成分对细胞损伤和 IL6/STAT3 信号传导的影响。最后，采用4%牛磺胆酸钠（NaT）诱导AP模型，评估SMI治疗AP的作用，验证潜在的分子机制。
结果：通过检索 TCMSP 和 ETCM 数据库，获得了 119 个 SMI 候选成分。UHPLC-QTOF/MS分析成功确定了SMI的代表性成分：人参皂甙Rb1、人参皂甙Rg1、人参皂甙Re和麦冬素D。获得15个中心靶点和8个相关通路，建立主要药理学网络。子网分析和分子对接表明，这四个主要 SMI 成分的作用主要与白细胞介素 (IL) 6/STAT3 通路有关。在体外，SMI、人参皂甙 Rb1、人参皂甙 Rg1、人参皂甙 Re 和麦冬素 D 增加了 NaT 刺激的小鼠胰腺腺泡 266-6 细胞的细胞活力并降低了 IL6 和 STAT3 的表达。体内，
结论：本研究表明，SMI可能通过抑制IL6/STAT3的活化发挥抗AP的抗炎作用，为其在临床实践中的潜在应用和进一步研究AP治疗提供依据。
更新日期：2022-08-02
Methods: Network pharmacology analysis and molecular docking based on identified components were performed to construct the potential therapeutic targets and pathways. The principal components of SMI were detected via ultra-high-performance liquid chromatography-coupled with quadrupole time-of-flight mass spectrometry (UHPLC-QTOF/MS). Effect of SMI and the identified components on cellular injury and IL6/STAT3 signaling was assessed on mouse pancreatic acinar cell line 266– 6 cells. Finally, 4% sodium taurocholate (NaT) was used to induce AP model to assess the effects of SMI in treating AP and validate the potential molecular mechanisms.
Results: By searching the TCMSP and ETCM databases, 119 candidate components of SMI were obtained. UHPLC-QTOF/MS analysis successfully determined the representative components of SMI: ginsenoside Rb1, ginsenoside Rg1, ginsenoside Re, and ophiopogonin D. Fifteen hub targets and eight related pathways were obtained to establish the main pharmacology network. Subnetwork analysis and molecular docking indicated that the effects of these four main SMI components were mostly related to the interleukin (IL) 6/STAT3 pathway. In vitro, SMI, ginsenoside Rb1, ginsenoside Rg1, ginsenoside Re, and ophiopogonin D increased the cell viability of NaT-stimulated mouse pancreatic acinar 266– 6 cells and decreased IL6 and STAT3 expression. In vivo, 10 mL/kg SMI significantly alleviated the pancreatic histopathological changes and the expression of IL6 and STAT3 in the AP mice.
Conclusion: This study demonstrated SMI may exert anti-inflammatory effects against AP by suppressing IL6/STAT3 activation, thus providing a basis for its potential use in clinical practice and further study in treating AP.
中文翻译：
参麦注射液治疗急性胰腺炎的抗炎作用及分子机制：网络药理分析与实验验证
背景：急性胰腺炎（AP）是一种未经特殊治疗的胰腺外分泌炎症性疾病。据报道参麦注射液 (SMI) 可消除实验性 AP 的严重性。本研究旨在基于网络药理学和实验验证，探索 SMI 对 AP 的协同保护作用的机制。
方法：进行基于已识别成分的网络药理学分析和分子对接，以构建潜在的治疗靶点和途径。通过超高效液相色谱-四极杆飞行时间质谱联用 (UHPLC-QTOF/MS) 检测 SMI 的主要成分。在小鼠胰腺腺泡细胞系 266-6 细胞上评估 SMI 和已识别成分对细胞损伤和 IL6/STAT3 信号传导的影响。最后，采用4%牛磺胆酸钠（NaT）诱导AP模型，评估SMI治疗AP的作用，验证潜在的分子机制。
结果：通过检索 TCMSP 和 ETCM 数据库，获得了 119 个 SMI 候选成分。UHPLC-QTOF/MS分析成功确定了SMI的代表性成分：人参皂甙Rb1、人参皂甙Rg1、人参皂甙Re和麦冬素D。获得15个中心靶点和8个相关通路，建立主要药理学网络。子网分析和分子对接表明，这四个主要 SMI 成分的作用主要与白细胞介素 (IL) 6/STAT3 通路有关。在体外，SMI、人参皂甙 Rb1、人参皂甙 Rg1、人参皂甙 Re 和麦冬素 D 增加了 NaT 刺激的小鼠胰腺腺泡 266-6 细胞的细胞活力并降低了 IL6 和 STAT3 的表达。体内，
结论：本研究表明，SMI可能通过抑制IL6/STAT3的活化发挥抗AP的抗炎作用，为其在临床实践中的潜在应用和进一步研究AP治疗提供依据。
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