Ischemia-reperfusion (I/R) injury is a progressive injury that aggravates the pathological state when the organ tissue restores blood supply after a certain period of ischemia, including the myocardial, brain, liver, kidney, and intestinal. With growing evidence that microRNAs (miRNAs) play an important role as posttranscription gene silencing mediators in many I/R injury, in this review, we highlight the microRNAs that are related to I/R injury and their regulatory molecular pathways. In addition, we discussed the potential role of miRNA as a biomarker and its role as a target in I/R injury treatment. Developing miRNAs are not without its challenges, but prudent design combined with existing clinical treatments will result in more effective therapies for I/R injury. This review is aimed at providing new research results obtained in this research field. It is hoped that new research on this topic will not only generate new insights into the pathophysiology of miRNA in I/R injury but also can provide a basis for the clinical application of miRNA in I/R.

To assess the effectiveness of electroacupuncture (EA) with rehabilitation training in reducing limb spasticity in post-stroke patients. A systematic review was performed by electronically searchin...

In recent years, the efficacy of electroacupuncture (EA) pretreatment generating ischemic tolerance mimicking ischemic pretreatment (IP) has been continuously confirmed, which was first found in the brain and then in the heart. Furthermore, researchers have observed the intensive cardioprotection impact of EA pretreatment on patients undergoing percutaneous coronary intervention (PCI) and heart valve replacement, indicating that EA pretreatment tends to be a valuable and advantageous avenue for preventing acute myocardial ischemia/reperfusion (I/R) injury or treatment of ischemic heart disease (IHD). In reality, the heart protection mechanism of EA pretreatment is robust and pleiotropic, of which the regulatory molecular pathways are involved in multichannel, multilevel, and multitarget, including energy metabolism, inflammatory response, calcium overload, oxidative stress, autophagy, and apoptosis. Through a growing number of clinical tests and basic experiments with animal models, researchers progressively explored the optimal acupoints and parameters, where EA pretreatment induced acute and delayed ischemic tolerance for myocardial protection. Thereby, this article aims to collect the relevant evidence on EA pretreatment against myocardial ischemia/reperfusion injury (MIRI) and summarize the mechanism of cardioprotection of EA pretreatment to provide ideas and methods for further clinical applications.

The brain-gut axis is a relatively recent discovery of a two-way regulation system between the gut and brain, suggesting that the gut microbiota may be a promising targeted prevention and treatment strategy for patients with a high risk of acute cerebral ischemia/reperfusion injury. There are many risk factors for ischemic stroke, and many studies have shown that the gut microbiota affects the absorption and metabolism of the body, as well as the risk factors of stroke, such as blood pressure, blood glucose, blood lipids, and atherosclerosis, either directly or indirectly. Furthermore, the gut microbiota can affect the occurrence and prognosis of ischemic stroke by regulating risk factors or immune responses. Therefore, this study aimed to collect evidence of the interaction between gut microbiota and ischemic stroke, summarize the interaction mechanism between the two, and explore the gut microbiota as a new targeted prevention and treatment strategy for patients with high ischemic risk.

Stroke is the leading cause of long-term disability in developed countries. Multitudinous evidence suggests that treadmill training treatment is beneficial for balance and stroke rehabilitation; however, the need for stroke therapy remains unmet. In the present study, a cerebral ischemia rat model was established by permanent middle cerebral artery occlusion (pMCAO) to explore the therapeutic effect and mechanism of scalp acupuncture combined with treadmill training on ischemic stroke. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and neuronal nuclear protein (NeuN) double staining and cellular inhibitor of apoptosis protein-1 (cIAP1) and NeuN immunofluorescence double staining were used to detect the short-term and long-term neuroprotective effects of scalp acupuncture combined with treadmill training on pMCAO rats. In addition, the antiapoptotic effect of the combined treatment was evaluated in pMCAO rats transfected with cIAP1 shRNA. Western blotting was used to detect the relative protein expression in the caspase-8/-9/-3 activation pathway downstream of cIAP1 to further clarify its regulatory mechanism. Our results showed that scalp acupuncture combined with treadmill training successfully achieved short-term and long-term functional improvement within 14 days after stroke, significantly inhibited neuronal apoptosis, and upregulated the expression of cIAP1 protein in the ischemic penumbra area of the ischemic brain. However, no significant functional improvement and antiapoptotic effect were found in pMCAO rats transfected with cIAP1 shRNA. Western blotting results showed that the combined therapy markedly inhibited the activation of the caspase-8/-9/-3 pathway. These findings indicate that scalp acupuncture combined with treadmill training therapy may serve as a more effective alternative modality in the treatment of ischemic stroke, playing an antiapoptotic role by upregulating the expression of cIAP1 and inhibiting the activation of the caspase-8/-9/-3 pathway.

Background: Musculoskeletal diseases (MSDs) are a common group of conditions involving bones, muscles, cartilage, ligaments, and nerves, which significantly impact patients’ quality of life and ability to participate in society. Anthocyanins (ACNs), as phytochemicals, possess various pharmacological and biological activities, including anti-apoptotic, antioxidant, anti-inflammatory, and immunosuppressive properties. In recent years, ACNs have shown remarkable potential in improving MSDs. This review article aims to recapitulate the therapeutic potential of ACNs and its mechanism of action in treating MSDs.Methods: Extensive literature was searched and reviewed through online electronic databases (PubMed, Embase, and Web of Science), focusing on analysing the specific roles and molecular mechanisms of ACNs in in vivo and in vitro studies.Results: ACNs exert protective effects on MSDs by targeting multiple key signaling pathways, including mitogen-activated protein kinase (MAPK), nuclear factor-kappaB (NF-κB), Wingless-related integration site (Wnt)/β-catenin, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), adenosyl monophosphate-dependent protein kinase (AMPK), receptor activator of nuclear factor-kappaΒ/receptor activator of nuclear factor-kappaB ligand/osteoprotegerin (RANK/RANKL/OPG) and oxidative stress signaling. In addition, ACNs exhibited anti-inflammatory, anti-apoptotic, and immunosuppressive properties. This article reviews the mechanisms and potential therapeutic applications of ACNs in the prevention and alleviation of MSDs, providing valuable reference points for further research and development of ACNs.Conclusion: ACNs improve the prevention of MSDs through multiple actions such as antioxidant, anti-inflammatory, immunomodulatory and bone metabolism homeostasis regulation. However, results from in vitro and in vivo studies still need to be further validated by human clinical trials.