OBJECTIVE：To systematically evaluate therape utic efficacy of Yixinshu preparation combined with conventional treatment plan for angina pectoris of coronary heart disease （CHD）vs. conventional treatment plan ，and to provide evidence-based reference for clinical drug use. METHODS ：Retrieved from Cochrane library ，PubMed，Embase，CBM，CNKI，Wanfang database and VIP ，randomized controlled trials （RCTs）about Yixinshu preparation combined with conventional treatment plan （trial group ） versus conventional treatment plan （control group ）for angina pectoris of coronary heart disease were collected during Jan. 1st in 2012 to Oct. 1st in 2020. After extracting the data ，the quality of included studies were evaluated with Cochrane System Evaluator Handbook 5.3；Meta-analysis was performed by using Stata 15.0 software. RESULTS ：A total of 23 RCTs involving 2 853 subjects were included. The results of Meta-analysis showed that the efficacy of angina pectoris [RR ＝0.92，95％CI（0.87，0.97），P＜0.05]， the times of angina pectoris attack [SMD ＝－0.98，95％CI（－1.09，－0.87），P＜0.05]，the duration of angina pectoris [SMD ＝ －0.77，95％CI（－0.88，－0.67），P＜0.05]，ECG curative effect [RR ＝0.91，95％CI（0.84，0.98），P＜0.05] and the improve rate of TCM syndromes [RR ＝0.89，95％CI（0.85，0.94），P＜0.05] in trial group were all better than control group ，with statistical significance. CONCLUSIONS ：Yixinshu preparation combined with conventional treatment plan is better than conventional treatment plan in terms of improving therapeutic efficacy of angina pectoris and ECG ，TCM syndrome improvement rate ，as well as reducing the frequency of angina pectoris attack ，angina pectoris attack duration.

Near-infrared (NIR)-light-triggered nanomedicine, including photodynamic therapy (PDT) and photothermal therapy (PTT), is growing an attractive approach for cancer therapy due to its high spatiotemporal controllability and minimal invasion, but the tumor eradication is limited by the intrinsic anti-stress response of tumor cells. Herein, we fabricate a tumor-microenvironment responsive CRISPR nanoplatform based on oxygen-deficient titania (TiO_2-x ) for mild NIR-phototherapy. In tumor microenvironment, the overexpressed hyaluronidase (HAase) and glutathione (GSH) can readily destroy hyaluronic acid (HA) and disulfide bond and releases the Cas9/sgRNA from TiO_2-x to target the stress alleviating regulators, i.e., nuclear factor E2-related factor 2 (NRF2) and heat shock protein 90α (HSP90α), thereby reducing the stress tolerance of tumor cells. Under subsequent NIR light illumination, the TiO_2-x demonstrates a higher anticancer effect both in vitro and in vivo. This strategy not only provides a promising modality to kills cancer cells in a minimal side-effects manner by interrupting anti-stress pathways but also proposes a general approach to achieve controllable gene editing in tumor region without unwanted genetic mutation in normal environments.

Hepatic stellate cells (HSCs) represent a significant component of hepatocellular carcinoma (HCC) microenvironments which play a critical role in tumor progression and drug resistance. Tumor-on-a-chip technology has provided a powerful in vitro platform to investigate the crosstalk between activated HSCs and HCC cells by mimicking physiological architecture with precise spatiotemporal control. Here we developed a tri-cell culture microfluidic chip to evaluate the impact of HSCs on HCC progression. On-chip analysis revealed activated HSCs contributed to endothelial invasion, HCC drug resistance and natural killer (NK) cell exhaustion. Cytokine array and RNA sequencing analysis were combined to indicate the iron-binding protein LIPOCALIN-2 (LCN-2) as a key factor in remodeling tumor microenvironments in the HCC-on-a-chip. LCN-2 targeted therapy demonstrated robust anti-tumor effects both in vitro 3D biomimetic chip and in vivo mouse model, including angiogenesis inhibition, sorafenib sensitivity promotion and NK-cell cytotoxicity enhancement. Taken together, the microfluidic platform exhibited obvious advantages in mimicking functional characteristics of tumor microenvironments and developing targeted therapies.

[This corrects the article DOI: 10.1016/j.apsb.2022.06.016.].