At present, due to the limitations of drug therapy targets for atherosclerosis, some patients fail to achieve satisfactory efficacy. Cholesterol efflux dysfunction and endothelial cell inflammation are considered to be important factors in the development of atherosclerosis. Peroxisome proliferator‐activated receptor gamma (PPARγ), a promising therapeutic target for atherosclerosis, plays a dual role in regulating cholesterol efflux and endothelial cell inflammation. However, the use of PPARγ agonist in clinical practice is greatly limited as it could lead to water and sodium retention and hence result in congestive heart failure. Qihuang Zhuyu Formula (QHZYF) is a hospital preparation of Jiangsu Province Hospital of Chinese Medicine which has definite effect in the treatment of atherosclerosis, but its pharmacological mechanism has not been clear. In this study, we successfully predicted that QHZYF might regulate cholesterol efflux and endothelial inflammation via targeting PPARγ‐mediated PPARγ/LXRα/ABCA1‐ABCG1 and PPARγ/NF‐κB p65 pathways by using UPLC‐Q‐TOF/MS, network pharmacology, bioinformatics analysis, and molecular docking technology. Subsequently, we confirmed in vivo that QHZYF could attenuate atherosclerosis in ApoE^−/− mice and regulate the expression levels of related molecules in PPARγ/LXRα/ABCA1‐ABCG1 and PPARγ/NF‐κB p65 pathways of ApoE^−/− mice and C57BL/6 wild‐type mice. Finally, in in vitro experiments, we found that QHZYF could reduce lipid content and increase cholesterol efflux rate of RAW 264.7 cells, inhibit the inflammatory response of HUVECs, and regulate the expression levels of related molecules in the two pathways. In addition, the above effects of QHZYF were significantly weakened after PPARγ knockdown in the two kinds of cells. In conclusion, our study revealed that QHZYF attenuates atherosclerosis via targeting PPARγ‐mediated PPARγ/LXRα/ABCA1‐ABCG1 and PPARγ/NF‐κB p65 pathways to regulate cholesterol efflux and endothelial cell inflammation. More importantly, our study offers a promising complementary and alternative therapy which is expected to make up for the limitation of current drug treatment methods and provide a valuable reference for new drugs development in the future.

Orthodontic tooth movement is linked to alveolar bone reconstruction. As a regulator of cell proliferation, insulin-like growth factor 1 (IGF-1) plays an important role in osteoporotic fracture healing. This study aims to investigate the effect of IGF-1 on alveolar bone remodeling in diabetic rats. Sprague Dawley (SD) rats were randomly divided into 3 groups, including a control group, a model group established with streptozotocin (STZ) injection to prepare the diabetic rats (type 1 diabetes), and an IGF-1 group of diabetic rats receiving daily intraperitoneal injections of 1.0 mg/kg IGF-1. Nickel-titanium coil springs were used to pull the first molar forward to establish the model. The maxillary first to third molars and the surrounding alveolar bone were collected to measure tooth movement distance. Hematoxylin and eosin (H&E) staining was applied to detect the pathological changes in the periodontal tissue. Real-time polymerase chain reaction (PCR) and western blot were adopted to measure bone morphogenetic protein 2 (BMP-2) mRNA and protein expression. Enzyme-linked immunosorbent assays (ELISAs) were used to measure interleukin-1α (IL-1α) levels in the serum. The tooth movement distance was significantly decreased, BMP-2 expression was downregulated, and IL-lα levels were enhanced in the model group compared to the control group (p < 0.05). However, the tooth movement distance was increased, BMP-2 expression was increased, and IL-lα levels were reduced in the IGF-1 group compared to the model group (p < 0.05). Hematoxylin and eosin staining showed that alveolar bone destruction was attenuated in the IGF-1 group, while the new bone was not active in the model group. Diabetes can damage alveolar bone remodeling in orthodontic tooth movement. The IGF-1 promotes alveolar bone remodeling by inhibiting inflammation and upregulating BMP-2 expression.

The incidence of coronary heart disease (CHD) complicated with anxiety or depression is increasing year by year. However, many anti-anxiety drugs or antidepressants have a certain degree of adverse reactions and are not easily accepted by patients. Xinkeshu (XKS), as a proprietary Chinese patent medicine with "psycho-cardiology" effect, is one of the commonly used drugs in the treatment of CHD complicated with anxiety or depression in China. To systematically evaluate the efficacy and safety of XKS for CHD complicated with anxiety or depression. Nine different electronic databases were independently searched to include randomized controlled trials (RCTs) of XKS for CHD complicated with anxiety or depression published from inception to February 2022, and the methodological quality was evaluated using the bias risk assessment tool from Cochrane Handbook 5.0 and the modified Jadad scale. Meta-analysis was performed using RevMan 5.3 and Stata 16.0 software. The GRADE Profiler 3.6.1 and TSA 0.9.5.10 beta were adopted to evaluate the certainty and conclusiveness of the evidence. A total of 18 RCTs involving 1907 subjects were included. There were 956 subjects in the XKS group and 951 subjects in the control group. Baseline conditions were consistent and comparable between the groups. Compared with single-use western medicine (WM), XKS combined with WM significantly reduced scores of Hamilton Anxiety Scale (HAMA) [Mean difference (MD) = -7.60, 95% confidence interval (95% CI) (-10.37, -4.83), P < 0.000 01], Zung Self-rating Anxiety Scale (SAS) [MD = -10.05, 95% CI (-12.70, -7.41), P < 0.000 01], Hamilton Depression Scale (HAMD) [MD = -6.74, 95% CI (-11.58, -1.90), P = 0.006], and Zung Self-rating Depression Scale (SDS) [MD = -10.75, 95% CI (-17.05,-4.45), P = 0.000 8], as well as improved clinical effective rate [odds ratio (OR) = 4.24, 95% CI (2.47, 7.27), P < 0.000 01]. In terms of safety, 4 studies reported the adverse reactions in detail. The severity was mild and symptoms disappeared after treatment. Current evidence indicates that XKS may be effective and safe in the treatment of patients with CHD complicated with anxiety or depression. Since the quality of the literature included in this study was generally low, there is an urgent need for more RCTs with high quality, low bias risk and sufficient sample size to validate our conclusions.

Aim of the Review. This study aims to summarize the therapeutic effect of luteolin on the pathogenesis of viral pneumonia, explore its absorption and metabolism in the human body, evaluate the possibility of luteolin as a drug to treat viral pneumonia, and provide a reference for future research. Materials and Methods. We searched MEDLINE/PubMed, Web of Science, China National Knowledge Infrastructure, and Google Scholar and collected research on luteolin in the treatment of viral pneumonia and related diseases since 2003. Then, we summarized the efficacy and potential of luteolin in directly inhibiting viral activity, limiting inflammatory storms, reducing pulmonary inflammation, and treating pneumonia complications. Results and Conclusion. Luteolin has the potential to treat viral pneumonia in multiple ways. Luteolin has a direct inhibitory effect on coronavirus, influenza virus, and respiratory syncytial virus. Luteolin can alleviate the inflammatory factor storm induced by multiple factors by inhibiting the function of macrophages or mast cells. Luteolin can reduce pulmonary inflammation, pulmonary edema, or pulmonary fibrosis induced by multiple factors. In addition, viral pneumonia may cause multisystem complications, while luteolin has extensive protective effects on the gastrointestinal system, cardiovascular system, and nervous system. However, due to the first-pass metabolism mediated by phase II enzymes, the bioavailability of oral luteolin is low. The bioavailability of luteolin can be improved, and its potential value can be further developed by changing the dosage form or route of administration.

Introduction: Myocardial Ischemia Reperfusion Injury (MIRI) contributes to adverse cardiovascular outcomes. Dysregulated myocardial autophagy plays a key role in MIRI, yet therapeutic strategies targeting this process are limited. Qihuang Zhuyu Formula (QHZYF), a traditional Chinese herbal compound, exhibits cardiovascular protective effects, but its molecular mechanism in MIRI remains unclear. The NF-κB P65/TRAIL signaling axis regulates autophagy in MIRI and may serve as a critical target for QHZYF intervention. Methods: QHZYF components were analyzed using UPLC-Q-TOF-MS. Network pharmacology identified the NF-κB P65/TRAIL pathway as a core mechanism. In vivo, a rat MIRI model was treated with QHZYF; myocardial injury was assessed via histology, electrocardiography, echocardiography, immunohistochemistry, western blot, and RT-qPCR. In vitro, H9C2 cells underwent hypoxia/reoxygenation and were treated with QHZYF. Autophagy and pathway-related markers, including NF-κB p65, TRAIL, Beclin 1, LC3, and P62, were measured. Results: Network pharmacology and experimental results confirmed that QHZYF targets NF-κB P65/TRAIL to restore myocardial autophagic homeostasis. Treatment reduced cardiomyocyte injury and normalized autophagy markers in both in vivo and in vitro models. Discussion: This study demonstrates that QHZYF exerts cardioprotective effects against MIRI by regulating autophagy and suppressing NF-κB P65/TRAIL signaling. Integration of compound analysis and experimental models revealed the pathway’s key role in autophagic imbalance and myocardial injury. QHZYF intervention restored autophagic homeostasis and mitigated cardiomyocyte damage, highlighting its potential application for MIRI prevention and therapy. Conclusion: QHZYF alleviates myocardial autophagy imbalance via the NF-κB P65/TRAIL pathway, providing mechanistic insight into its therapeutic potential in MIRI management.