Diabetes mellitus (DM) is a global health issue in the twenty-first century, and there are numerous challenges in preventing and alleviating its chronic complications. The herb Epimedium has beneficial therapeutic effects on various human diseases, including DM. Its major flavonoid component, icariin, has significant anti-DM activity and may help improve pancreatic β-cell dysfunction and insulin resistance. Furthermore, preclinical evidence has shown that icariin and its in vivo bioactive form, icariside II, have preventive and therapeutic effects on several diabetic complications, including diabetic cardiomyopathy, diabetic vascular endothelial disorder, diabetic nephropathy, and diabetic erectile dysfunction. In this review, we present the general and toxicological information concerning icariin and icariside II and review the anti-DM effects of icariin from a molecular perspective. Additionally, we discuss the potential benefits of icariin and icariside II on the important pathological mechanisms of various diabetic complications. Despite positive preclinical evidence, additional investigations are needed before relevant clinical studies can be conducted. Therefore, we conclude with suggestions for future research. Hopefully, this review will provide a comprehensive molecular perspective for future research and product development related to icariin and icariside II in treating DM and diabetic complications.

Existing comprehensive management strategies for COPD effectively relieve the symptoms of patients, delay the deterioration of lung function, and prevent the progression of COPD through various means and multidisciplinary interventions. However, there has been limited progress in therapies that address the underlying causes of COPD pathogenesis. Recent studies have identified specific changes in the gut and pulmonary microbiota in response to exposure to smoke that can cause or exacerbate CS-COPD by regulating the inflammatory immune response in the lungs through the gut-lung axis. As a convenient and controllable intervention, modifying the diet to include more dietary fiber can effectively improve the prognosis of CS-COPD. Gut microbiota ferment dietary fiber to produce short-chain fatty acids, which connect the microbial communities in the lung and gut mucosa across the gut-lung axis, playing an anti-inflammatory and immunosuppressive role in the lungs. Given that the effect of dietary fiber on gut microbiota was highly similar to that of quitting smoking on gut microbiota, we assume that microbiota might be a potential therapeutic target for dietary fiber to alleviate and prevent CS-COPD. This study examines the similarities between pulmonary and gut microbiota changes in the presence of smoking and dietary fiber. It also highlights the mechanism by which SCFAs link pulmonary and gut microbiota in CS-COPD and analyzes the anti-inflammatory and immunomodulatory effects of short-chain fatty acids on CS-COPD via the gut-lung axis.

Quercetin is a flavonoid with antioxidant and anti-inflammatory properties. Quercetin has potentially beneficial therapeutic effects for several diseases, including cigarette smoking–induced chronic obstructive pulmonary disease (CS-COPD). Many studies have shown that quercetin’s antioxidant and anti-inflammatory properties have positive therapeutic potential for CS-COPD. In addition, quercetin’s immunomodulatory, anti-cellular senescence, mitochondrial autophagy–modulating, and gut microbiota–modulating effects may also have therapeutic value for CS-COPD. However, there appears to be no review of the possible mechanisms of quercetin for treating CS-COPD. Moreover, the combination of quercetin with common therapeutic drugs for CS-COPD needs further refinement. Therefore, in this article, after introducing the definition and metabolism of quercetin, and its safety, we comprehensively presented the pathogenesis of CS-COPD related to oxidative stress, inflammation, immunity, cellular senescence, mitochondrial autophagy, and gut microbiota. We then reviewed quercetin’s anti-CS-COPD effects, performed by influencing these mechanisms. Finally, we explored the possibility of using quercetin with commonly used drugs for treating CS-COPD, providing a basis for future screening of excellent drug combinations for treating CS-COPD. This review has provided meaningful information on quercetin’s mechanisms and clinical use in treating CS-COPD.

A new variant named Omicron (B.1.1.529), first identified in South Africa, has become of considerable interest to the World Health Organization. This variant differs from the other known major variants, as it carries a large number of unusual mutations, particularly in the spinous process protein and receptor binding domains. Some specific mutation sites make it vaccine resistant, highly infectious, and highly pathogenic. The world fears that the Omicron variant could be even more harmful than the previous major variant, given that it has emerged amid fierce competition to trigger a new global pandemic peak as infections in South Africa rise. However, some epidemiological evidence has emerged that the Omicron variant may produce milder patient symptoms. We speculate if the virulence of the Omicron variant will diminish as transmissibility increases, thereby signaling the beginning of the end for the global COVID‐19 pandemic. Based on this view, we make recommendations for COVID‐19 mitigation in the present and future. However, it will take a few weeks to determine the true threat posed by the Omicron variant and we need to be fully prepared for future outbreaks, regardless of their severity.

Rheumatoid arthritis (RA) is an essential cause of secondary sarcopenia, and patients with RA face a higher risk of developing sarcopenia. In the literature, there is a lack of reviews on animal models of RA-related sarcopenia. This review examines sarcopenia-related changes and mechanisms in induced and immune-mediated arthritis animal models and highlights potential preclinical therapies. The mechanisms for developing sarcopenia in these animal models involved inflammation, protein degradation pathways, protein synthesis, muscle regeneration and differentiation, oxidative stress, energy metabolism, and amino acid metabolism. Some anti-rheumatic drugs, supplements and nutrients, antioxidants, and physical therapy and training have been shown to improve muscle atrophy, maintain muscle mass, and prevent grip strength loss in different RA-related sarcopenia animal models. Overall, this review aims to deepen the mechanistic understanding of RA-related sarcopenia and provide a basis for developing innovative therapies.