Video_3_Hemifacial spasm caused by unruptured fusiform vertebral aneurysm treated with endovascular coil embolization: a case report.MOV

Hemifacial spasm due to fusiform aneurysm of the vertebral artery is extremely rare. The lateral spread response (LSR) is routinely used to monitor hemifacial spasms during microvascular decompression to predict the degree of postoperative remission of hemifacial spasm. We report a case of hemifacial spasm caused by an unruptured fusiform vertebral aneurysm treated with intravascular intervention and monitoring of LSR. A 59-year-old man was admitted to the hospital with a left facial spasm that gradually worsened for 1 year. Preoperative cerebrovascular angiography indicated fusiform aneurysms in the intracranial segment of the left vertebral artery close to the left facial nerve. The patient underwent parent artery occlusion and aneurysm embolization, and LSR was monitored intraoperatively. After intraoperative aneurysm embolization, LSR disappeared immediately. The postoperative review of cerebrovascular angiography indicated that the parent artery and aneurysm were embolized successfully, and the patient's left facial spasm was relieved after surgery. Hemifacial spasm caused by the vertebral artery fusiform aneurysm can be safely and effectively treated by parent artery occlusion and aneurysm embolization. Meanwhile, intraoperative LSR monitoring can be used to predict postoperative efficacy.</p

Video_2_Hemifacial spasm caused by unruptured fusiform vertebral aneurysm treated with endovascular coil embolization: a case report.MOV

Hemifacial spasm due to fusiform aneurysm of the vertebral artery is extremely rare. The lateral spread response (LSR) is routinely used to monitor hemifacial spasms during microvascular decompression to predict the degree of postoperative remission of hemifacial spasm. We report a case of hemifacial spasm caused by an unruptured fusiform vertebral aneurysm treated with intravascular intervention and monitoring of LSR. A 59-year-old man was admitted to the hospital with a left facial spasm that gradually worsened for 1 year. Preoperative cerebrovascular angiography indicated fusiform aneurysms in the intracranial segment of the left vertebral artery close to the left facial nerve. The patient underwent parent artery occlusion and aneurysm embolization, and LSR was monitored intraoperatively. After intraoperative aneurysm embolization, LSR disappeared immediately. The postoperative review of cerebrovascular angiography indicated that the parent artery and aneurysm were embolized successfully, and the patient's left facial spasm was relieved after surgery. Hemifacial spasm caused by the vertebral artery fusiform aneurysm can be safely and effectively treated by parent artery occlusion and aneurysm embolization. Meanwhile, intraoperative LSR monitoring can be used to predict postoperative efficacy.</p

Video_1_Hemifacial spasm caused by unruptured fusiform vertebral aneurysm treated with endovascular coil embolization: a case report.MOV

Hemifacial spasm due to fusiform aneurysm of the vertebral artery is extremely rare. The lateral spread response (LSR) is routinely used to monitor hemifacial spasms during microvascular decompression to predict the degree of postoperative remission of hemifacial spasm. We report a case of hemifacial spasm caused by an unruptured fusiform vertebral aneurysm treated with intravascular intervention and monitoring of LSR. A 59-year-old man was admitted to the hospital with a left facial spasm that gradually worsened for 1 year. Preoperative cerebrovascular angiography indicated fusiform aneurysms in the intracranial segment of the left vertebral artery close to the left facial nerve. The patient underwent parent artery occlusion and aneurysm embolization, and LSR was monitored intraoperatively. After intraoperative aneurysm embolization, LSR disappeared immediately. The postoperative review of cerebrovascular angiography indicated that the parent artery and aneurysm were embolized successfully, and the patient's left facial spasm was relieved after surgery. Hemifacial spasm caused by the vertebral artery fusiform aneurysm can be safely and effectively treated by parent artery occlusion and aneurysm embolization. Meanwhile, intraoperative LSR monitoring can be used to predict postoperative efficacy.</p

Video_4_Hemifacial spasm caused by unruptured fusiform vertebral aneurysm treated with endovascular coil embolization: a case report.MP4

Hemifacial spasm due to fusiform aneurysm of the vertebral artery is extremely rare. The lateral spread response (LSR) is routinely used to monitor hemifacial spasms during microvascular decompression to predict the degree of postoperative remission of hemifacial spasm. We report a case of hemifacial spasm caused by an unruptured fusiform vertebral aneurysm treated with intravascular intervention and monitoring of LSR. A 59-year-old man was admitted to the hospital with a left facial spasm that gradually worsened for 1 year. Preoperative cerebrovascular angiography indicated fusiform aneurysms in the intracranial segment of the left vertebral artery close to the left facial nerve. The patient underwent parent artery occlusion and aneurysm embolization, and LSR was monitored intraoperatively. After intraoperative aneurysm embolization, LSR disappeared immediately. The postoperative review of cerebrovascular angiography indicated that the parent artery and aneurysm were embolized successfully, and the patient's left facial spasm was relieved after surgery. Hemifacial spasm caused by the vertebral artery fusiform aneurysm can be safely and effectively treated by parent artery occlusion and aneurysm embolization. Meanwhile, intraoperative LSR monitoring can be used to predict postoperative efficacy.</p

Table13_Nephroprotective mechanisms of Rhizoma Chuanxiong and Radix et Rhizoma Rhei against acute renal injury and renal fibrosis based on network pharmacology and experimental validation.XLSX

The molecular mechanisms of Rhizoma Chuanxiong (Chuanxiong, CX) and Rhei Radix et Rhizoma (Dahuang, DH) in treating acute kidney injury (AKI) and subsequent renal fibrosis (RF) were investigated in this study by applying network pharmacology and experimental validation. The results showed that aloe-emodin, (−)-catechin, beta-sitosterol, and folic acid were the core active ingredients, and TP53, AKT1, CSF1R, and TGFBR1 were the core target genes. Enrichment analyses showed that the key signaling pathways were the MAPK and IL-17 signaling pathways. In vivo experiments confirmed that Chuanxiong and Dahuang pretreatments significantly inhibited the levels of SCr, BUN, UNAG, and UGGT in contrast media-induced acute kidney injury (CIAKI) rats (p < 0.001). The results of Western blotting showed that compared with the control group, the protein levels of p-p38/p38 MAPK, p53, and Bax in the contrast media-induced acute kidney injury group were significantly increased, and the levels of Bcl-2 were significantly reduced (p < 0.001). Chuanxiong and Dahuang interventions significantly reversed the expression levels of these proteins (p < 0.01). The localization and quantification of p-p53 expression in immunohistochemistry technology also support the aforementioned results. In conclusion, our data also suggest that Chuanxiong and Dahuang may inhibit tubular epithelial cell apoptosis and improve acute kidney injury and renal fibrosis by inhibiting p38 MAPK/p53 signaling.</p

Table1_Nephroprotective mechanisms of Rhizoma Chuanxiong and Radix et Rhizoma Rhei against acute renal injury and renal fibrosis based on network pharmacology and experimental validation.XLSX

The molecular mechanisms of Rhizoma Chuanxiong (Chuanxiong, CX) and Rhei Radix et Rhizoma (Dahuang, DH) in treating acute kidney injury (AKI) and subsequent renal fibrosis (RF) were investigated in this study by applying network pharmacology and experimental validation. The results showed that aloe-emodin, (−)-catechin, beta-sitosterol, and folic acid were the core active ingredients, and TP53, AKT1, CSF1R, and TGFBR1 were the core target genes. Enrichment analyses showed that the key signaling pathways were the MAPK and IL-17 signaling pathways. In vivo experiments confirmed that Chuanxiong and Dahuang pretreatments significantly inhibited the levels of SCr, BUN, UNAG, and UGGT in contrast media-induced acute kidney injury (CIAKI) rats (p < 0.001). The results of Western blotting showed that compared with the control group, the protein levels of p-p38/p38 MAPK, p53, and Bax in the contrast media-induced acute kidney injury group were significantly increased, and the levels of Bcl-2 were significantly reduced (p < 0.001). Chuanxiong and Dahuang interventions significantly reversed the expression levels of these proteins (p < 0.01). The localization and quantification of p-p53 expression in immunohistochemistry technology also support the aforementioned results. In conclusion, our data also suggest that Chuanxiong and Dahuang may inhibit tubular epithelial cell apoptosis and improve acute kidney injury and renal fibrosis by inhibiting p38 MAPK/p53 signaling.</p

Table4_Nephroprotective mechanisms of Rhizoma Chuanxiong and Radix et Rhizoma Rhei against acute renal injury and renal fibrosis based on network pharmacology and experimental validation.XLSX

The molecular mechanisms of Rhizoma Chuanxiong (Chuanxiong, CX) and Rhei Radix et Rhizoma (Dahuang, DH) in treating acute kidney injury (AKI) and subsequent renal fibrosis (RF) were investigated in this study by applying network pharmacology and experimental validation. The results showed that aloe-emodin, (−)-catechin, beta-sitosterol, and folic acid were the core active ingredients, and TP53, AKT1, CSF1R, and TGFBR1 were the core target genes. Enrichment analyses showed that the key signaling pathways were the MAPK and IL-17 signaling pathways. In vivo experiments confirmed that Chuanxiong and Dahuang pretreatments significantly inhibited the levels of SCr, BUN, UNAG, and UGGT in contrast media-induced acute kidney injury (CIAKI) rats (p < 0.001). The results of Western blotting showed that compared with the control group, the protein levels of p-p38/p38 MAPK, p53, and Bax in the contrast media-induced acute kidney injury group were significantly increased, and the levels of Bcl-2 were significantly reduced (p < 0.001). Chuanxiong and Dahuang interventions significantly reversed the expression levels of these proteins (p < 0.01). The localization and quantification of p-p53 expression in immunohistochemistry technology also support the aforementioned results. In conclusion, our data also suggest that Chuanxiong and Dahuang may inhibit tubular epithelial cell apoptosis and improve acute kidney injury and renal fibrosis by inhibiting p38 MAPK/p53 signaling.</p

DataSheet3_Nephroprotective mechanisms of Rhizoma Chuanxiong and Radix et Rhizoma Rhei against acute renal injury and renal fibrosis based on network pharmacology and experimental validation.CSV

The molecular mechanisms of Rhizoma Chuanxiong (Chuanxiong, CX) and Rhei Radix et Rhizoma (Dahuang, DH) in treating acute kidney injury (AKI) and subsequent renal fibrosis (RF) were investigated in this study by applying network pharmacology and experimental validation. The results showed that aloe-emodin, (−)-catechin, beta-sitosterol, and folic acid were the core active ingredients, and TP53, AKT1, CSF1R, and TGFBR1 were the core target genes. Enrichment analyses showed that the key signaling pathways were the MAPK and IL-17 signaling pathways. In vivo experiments confirmed that Chuanxiong and Dahuang pretreatments significantly inhibited the levels of SCr, BUN, UNAG, and UGGT in contrast media-induced acute kidney injury (CIAKI) rats (p < 0.001). The results of Western blotting showed that compared with the control group, the protein levels of p-p38/p38 MAPK, p53, and Bax in the contrast media-induced acute kidney injury group were significantly increased, and the levels of Bcl-2 were significantly reduced (p < 0.001). Chuanxiong and Dahuang interventions significantly reversed the expression levels of these proteins (p < 0.01). The localization and quantification of p-p53 expression in immunohistochemistry technology also support the aforementioned results. In conclusion, our data also suggest that Chuanxiong and Dahuang may inhibit tubular epithelial cell apoptosis and improve acute kidney injury and renal fibrosis by inhibiting p38 MAPK/p53 signaling.</p

Table15_Nephroprotective mechanisms of Rhizoma Chuanxiong and Radix et Rhizoma Rhei against acute renal injury and renal fibrosis based on network pharmacology and experimental validation.DOCX

The molecular mechanisms of Rhizoma Chuanxiong (Chuanxiong, CX) and Rhei Radix et Rhizoma (Dahuang, DH) in treating acute kidney injury (AKI) and subsequent renal fibrosis (RF) were investigated in this study by applying network pharmacology and experimental validation. The results showed that aloe-emodin, (−)-catechin, beta-sitosterol, and folic acid were the core active ingredients, and TP53, AKT1, CSF1R, and TGFBR1 were the core target genes. Enrichment analyses showed that the key signaling pathways were the MAPK and IL-17 signaling pathways. In vivo experiments confirmed that Chuanxiong and Dahuang pretreatments significantly inhibited the levels of SCr, BUN, UNAG, and UGGT in contrast media-induced acute kidney injury (CIAKI) rats (p < 0.001). The results of Western blotting showed that compared with the control group, the protein levels of p-p38/p38 MAPK, p53, and Bax in the contrast media-induced acute kidney injury group were significantly increased, and the levels of Bcl-2 were significantly reduced (p < 0.001). Chuanxiong and Dahuang interventions significantly reversed the expression levels of these proteins (p < 0.01). The localization and quantification of p-p53 expression in immunohistochemistry technology also support the aforementioned results. In conclusion, our data also suggest that Chuanxiong and Dahuang may inhibit tubular epithelial cell apoptosis and improve acute kidney injury and renal fibrosis by inhibiting p38 MAPK/p53 signaling.</p

Table3_Nephroprotective mechanisms of Rhizoma Chuanxiong and Radix et Rhizoma Rhei against acute renal injury and renal fibrosis based on network pharmacology and experimental validation.XLSX

The molecular mechanisms of Rhizoma Chuanxiong (Chuanxiong, CX) and Rhei Radix et Rhizoma (Dahuang, DH) in treating acute kidney injury (AKI) and subsequent renal fibrosis (RF) were investigated in this study by applying network pharmacology and experimental validation. The results showed that aloe-emodin, (−)-catechin, beta-sitosterol, and folic acid were the core active ingredients, and TP53, AKT1, CSF1R, and TGFBR1 were the core target genes. Enrichment analyses showed that the key signaling pathways were the MAPK and IL-17 signaling pathways. In vivo experiments confirmed that Chuanxiong and Dahuang pretreatments significantly inhibited the levels of SCr, BUN, UNAG, and UGGT in contrast media-induced acute kidney injury (CIAKI) rats (p < 0.001). The results of Western blotting showed that compared with the control group, the protein levels of p-p38/p38 MAPK, p53, and Bax in the contrast media-induced acute kidney injury group were significantly increased, and the levels of Bcl-2 were significantly reduced (p < 0.001). Chuanxiong and Dahuang interventions significantly reversed the expression levels of these proteins (p < 0.01). The localization and quantification of p-p53 expression in immunohistochemistry technology also support the aforementioned results. In conclusion, our data also suggest that Chuanxiong and Dahuang may inhibit tubular epithelial cell apoptosis and improve acute kidney injury and renal fibrosis by inhibiting p38 MAPK/p53 signaling.</p