Efficacy and safety of Buyang Huanwu Decoction in patients with spinal cord injury: A meta-analysis of randomized controlled trials.

BACKGROUND: There has been growing interest in using the traditional Chinese herb Buyang Huanwu Decoction (BHD) as a potential treatment for spinal cord injury (SCI), owing to its long-used treatment for SCI in China. However, the efficacy and safety of BHD treatment for SCI remain widely skeptical. This meta-analysis aims to assess the safety and efficacy of BHD in managing SCI. METHOD: A comprehensive literature search was conducted across several databases, including PubMed, EMBASE, Cochrane Library, CNKI, Wanfang, VIP, and Sinomed, up to January 1, 2024. Randomized controlled clinical trials evaluating the safety or efficacy of BHD in SCI treatment were included. The analysis focused on 8 critical endpoints: Patient-perceived total clinical effective rate, American Spinal Cord Injury Association (ASIA) sensory score, ASIA motor score, somatosensory evoked potential, motor evoked potential, visual analog scale pain score, Japanese Orthopaedic Association score, and adverse events. RESULTS: Thirteen studies comprising 815 participants met the inclusion criteria. No significant heterogeneity or publication bias was observed across the trials. The findings revealed significant improvements in the patient-perceived total clinical effective rate (OR = 3.77; 95% confidence interval [CI] = [2.43, 5.86]; P < .001), ASIA sensory score (mean difference [MD] = 8.22; 95% CI = [5.87, 10.56]; P < .001), ASIA motor score (MD = 7.16; 95% CI = [5.15, 9.18]; P < .001), somatosensory evoked potential (MD = 0.25; 95% CI = [0.03, 0.48]; P = .02), motor evoked potential (MD = 0.30; 95% CI = [0.14, 0.46]; P = .0002), and Japanese Orthopaedic Association score (MD = 1.99; 95% CI = [0.39, 3.58]; P = .01) in the BHD combination group compared to the control group. Additionally, there was a significant reduction in visual analog scale pain scores (MD = -0.81; 95% CI = [-1.52, -0.11]; P = .02) with BHD combination treatment, without a significant increase in adverse effects (OR = 0.68; 95% CI = [0.33, 1.41]; P = .3). CONCLUSION: The current evidence suggests that BHD is effective and safe in treating SCI, warranting consideration as a complementary and alternative therapy. However, given the low methodological quality of the included studies, further rigorous research is warranted to validate these findings.

LDB2 inhibits proliferation and migration in liver cancer cells by abrogating HEY1 expression.

Hepatocellular carcinoma (HCC) was one of the most common cancers around the world, has very low 5-year survival rate. However, the mechanism of HCC occurrence and development is largely unknown. LDB2 belongs to the LIM-domain binding family and functions as an adaptor for transcriptional regulation. Here we found that LDB2 is downregulated in HCC samples. LDB2 has the ability to inhibit proliferation and migration of hepatocarcinoma cells. We found that the proliferation and migration abilities in HCC sample cells were impaired after LDB2 overexpression and vice versa. In mechanism, we found that LDB2 can recruit BRD7 to HEY1 promoter and then block its expression. HEY1 whose expression is upregulated in HCC acts as an oncogene. In brief, our research reveals a new regulatory mechanism for hepatocarcinoma cell proliferation and migration.

Inhibition on Numb/Notch signal pathway enhances radiosensitivity of lung cancer cell line H358.

The objective of the study is to investigate the effects of the Numb/Notch signal pathway on the radiosensitivity of lung cancer cell line H358. MTT assay and colony forming assay were used to detect the effects of different doses of X-rays and MW167 on the in vitro proliferation of the lung cancer cell line H358. Flow cytometry was applied to evaluate the effects of X rays on the apoptosis of H358. Scratch assay and Transwell invasion assay were used to examine the effects of X-rays on the migration and invasion abilities of H358. The mRNA and protein expressions in the signal pathway were detected by real-time PCR and western blot. Assays in vitro confirmed the effects of the Numb/Notch pathway inhibitor on the radiosensitivity to lung cancer. MW167 enhanced the inhibiting effects of X-ray on the proliferation of H358 cell line. After the addition of MW167, the apoptosis rates significantly increased, but the invasion and migration abilities decreased significantly. Meanwhile, MW167 could dose-dependently promote the increase of expression of Numb, which is the upstream gene of the Numb/Notch signaling pathway, but inhibit the expression of and HES1. In vivo experiments revealed that cell proliferation was suppressed in the radiation, pathway inhibitor, and pathway inhibitor + radiation groups, and the pathway inhibitor + radiation group exhibited more active anti-tumor ability when compared with the blank group (all P < 0.05); Numb expression was up-regulated, but Notch1 and HES1 expressions were down-regulated in those three groups, and also, the pathway inhibitor + radiation group exhibited more significant alternation when compared with the blank group (all P < 0.05); cell apoptosis was promoted in those three groups, and the pathway inhibitor + radiation group showed more active apoptosis when compared with the blank group (all P < 0.05). Repression of the Numb/Notch pathway enhances the effects of radiotherapy on the radiosensitivity of the lung cancer cell line H358, and thus the Numb/Notch pathway may be a new target of radiotherapy for lung cancer.

MicroRNA-322 protects hypoxia-induced apoptosis in cardiomyocytes via BDNF gene.

BACKGROUND: Cardiomyocytes apoptosis under hypoxia condition contributes significantly to various cardiovascular diseases. In this study, we investigated the role of microRNA-322 (miR-322) in regulating hypoxia-induced apoptosis in neonatal murine cardiomyocytes in vitro. METHOD: Cardiomyocytes of C57BL/6J mice were treated with hypoxia condition in vitro. Cardiomyocyte apoptosis was measured by TUNEL assay. Gene expression pattern of miR-322 was measured by qRT-PCR. Stable downregulation of miR-322 in cardiomyocytes were achieved by lentiviral transduction, and the effect of miR-322 downregulation on hypoxia-induced cardiomyocyte apoptosis was investigated. Possible regulation of miR-322 on its downstream target gene, brain derived neurotrophic factor (BDNF) was investigated in cardiomyocytes. BDNF was then genetically silenced by siRNA to evaluate its role in miR-137 mediated cardiomyocyte apoptosis protection under hypoxia condition. RESULTS: Under hypoxia condition, significant apoptosis was induced and miR-322 was significantly upregulated in cardiomyocytes in vitro. Through lentiviral transduction, miR-322 was efficiently knocked down in cardiomyocytes. Downregulation of miR-322 protected hypoxia-induced cardiomyocyte apoptosis. Luciferase assay showed BDNF was the target gene of miR-322. QRT-PCR showed BDNF expression was associated with miR-322 regulation on hypoxia-induced cardiomyocyte apoptosis. Silencing BDNF in cardiomyocyte through siRNA transfection reversed the protective effect of miR-322 downregulation on hypoxia-induced apoptosis. CONCLUSION: Our study revealed that miR-322, in association with BDNF, played important role in regulating hypoxia-induced apoptosis in cardiomyocyte.

Nonangiogenic function of VEGF and enhanced radiosensitivity of HeLa cells by inhibition of VEGF expression.

Vascular endothelial growth factor (VEGF) plays an important role in the initiation and regulation of angiogenesis in various tumor tissues. Recently, several therapeutic approaches based on the inhibition of VEGF function during angiogenesis. However, VEGF function in cervical cancer may not be limited to angiogenesis, and VEGF signaling may be important for the ability of these tumor cells to evade apoptosis and progress towards invasive and metastatic diseases. In our study, VEGF expression was knocked down using plasmid-based RNA interference (RNAi) and detected in cervical carcinoma cells using real-time RT-PCR to screen the best RNA interference plasmid and reveal the VEGF expression level by radiation. Cell apoptosis and tumor xenografts in nude mice were measured by flow cytometry and immunohistochemistry, respectively, to further verify the possibility of enhancing apoptosis and radiosensitivity of cervical carcinoma cells by inhibition of VEGF expression. VEGF expression was significantly inhibited and the apoptosis was efficiently increased by RNAi. Moreover, the expression of VEGF was increased in HeLa cells in vivo and in vitro only by radiation. Increased apoptotic cell death and knockdown of VEGF expression in HeLa cells indicated increased cellular sensitivity to radiation. The data suggested that inhibited VEGF expression enhances radiosensitivity in cervical cancer therapy.