Resveratrol and quercetin, widely found in foods and vegetables, are plant polyphenols reported to have a wide range of biological activities. Despite their limited bioavailabilities, both resveratrol and quercetin are known to exhibit anti-inflammation and anti-obesity effects. We hypothesized that gut microbiota may be a potential target for resveratrol and quercetin to prevent the development of obesity. The aim of this research was to confirm whether a combination of quercetin and resveratrol (CQR) could restore the gut microbiota dysbiosis induced by a high-fat diet (HFD). In this study, Wistar rats were divided into three groups: a normal diet (ND) group, a HFD group and a CQR group. The CQR group was treated with a HFD and administered with a combination of quercetin [30 mg per kg body weight (BW) per day] and resveratrol [15 mg per kg body weight (BW) per day] by oral gavage. At the end of 10 weeks, CQR reduced the body weight gain and visceral (epididymal, perirenal) adipose tissue weight. Moreover, CQR also reduced serum lipids, attenuated serum inflammatory markers [interleukin (IL)-6, tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1] and reversed serum biochemical parameters (adiponectin, insulin, leptin, etc.). Importantly, our results demonstrated that CQR could modulate the gut microbiota composition. 16S rRNA gene sequencing revealed that CQR had an impact on gut microbiota, decreasing Firmicutes (P < 0.05) and the proportion of Firmicutes to Bacteroidetes (P = 0.052). CQR also significantly inhibited the relative abundance of Desulfovibrionaceae (P < 0.01), Acidaminococcaceae (P < 0.05), Coriobacteriaceae (P < 0.05), Bilophila (P < 0.05), Lachnospiraceae (P < 0.05) and its genus Lachnoclostridium (P < 0.001), which were reported to be potentially related to diet-induced obesity. Moreover, compared with the HFD group, the relative abundance of Bacteroidales_S24-7_group (P < 0.01), Christensenellaceae (P < 0.001), Akkermansia (P < 0.01), Ruminococcaceae (P < 0.01) and its genera Ruminococcaceae_UCG-014 (P < 0.01), and Ruminococcaceae_UCG-005 (P < 0.01), which were reported to have an effect of relieving HFD-induced obesity, was markedly increased in the CQR group. Overall, these results indicated that administration of CQR may have beneficial effects on ameliorating HFD-induced obesity and reducing HFD-induced gut microbiota dysbiosis.

As one of major chronic complications of diabetes, diabetic foot ulcer (DFU) is the main cause of disability and death. The clinical diagnosis and prognosis of DFU is inadequate. For clinicians, if the risk stratification of DFU can be obtained earlier in diabetic patients, the hospitalization, disability and mortality rate will be reduced. In addition to the inflammatory biomarkers that have been widely concerned and used, e.g., procalcitonin, pentraxin-3, C-reactive protein (CRP), interleukins (ILs), and tumor necrosis factor-α (TNF-α), etc., a more comprehensive prediction of the risk and severity of DFU is needed to reflect new biomarkers for therapeutic intervention effects. Along with the development of systems biology technology, genomics, proteomics, metabolomics and microbiome have been used in the studies on DFU for better understanding of the disease. In this review, new biomarkers that are expected to assist in the accurate diagnosis and risk stratification of DFU will be discussed and summarized in detail.

Diabetic ulcers are one of the major complications of diabetes, and patients usually suffer from amputation and death due to delayed ulcer wound healing. Persistent inflammation and oxidative stress at the wound site are the main manifestations of delayed wound healing in diabetic ulcers. In addition, chronic hyperglycemia in patients can lead to circulatory accumulation of lipid peroxidation products and impaired iron metabolism pathways leading to the presence of multiple free irons in plasma. Ferroptosis, a newly discovered form of cell death, is characterized by intracellular iron overload and accumulation of iron-dependent lipid peroxides. These indicate that ferroptosis is one of the potential mechanisms of delayed wound healing in diabetic ulcers and will hopefully be a novel therapeutic target for delayed wound healing in diabetic patients. This review explored the pathogenesis of diabetic ulcer wound healing, reveals that oxidative stress and lipid peroxidation are common pathological mechanisms of ferroptosis and delayed wound healing in diabetic ulcers. Based on strong evidence, it is speculated that ferroptosis and diabetic ulcers are closely related, and have value of in-depth research. We attempted to clarify prospective associations between ferroptosis and diabetic ulcers in terms of GPX4, iron overload, ferroptosis inhibitors, AGEs, and HO-1, to provide new ideas for exploring the clinical treatment of diabetic ulcers.

Major depressive disorder (MDD) is a serious psychiatric disorder that associated with high rate of disability and increasing suicide rate, and the pathogenesis is still unclear. Many researches showed that the energy metabolism of patients with depression is impaired, which may be the direction of depression treatment. In this review, we focus on the "omics" technologies such as genomics, proteomics, transcriptomics and metabolomics, as well as imaging, and the progress on energy metabolism of MDD. These findings indicate that abnormal energy metabolism is one of the important mechanisms for the occurrence and development of depression. Although the research on various mechanisms of depression is still ongoing, the rapid development of new technologies and the joint use of various technologies will help to clarify the pathogenesis of depression and explore efficient diagnosis and treatment methods.

Gut microbiota dysbiosis has been implicated as a vital element in the development or exacerbation of mental disorders, such as major depressive disorder (MDD). Based on the current interest in the gut–brain axis, we investigate the effects of chlorogenic acid (CGA) on gut microbiota in a rat model of MDD. Depression was induced by the adrenocorticotropic hormone (ACTH, 100 μg per rat) in male Wistar rats, which were intervened with using saline or CGA (500 mg kg⁻¹). Behavioral changes and serum parameters were assessed and fecal samples were analyzed by 16S rRNA gene sequencing. Our studies demonstrated that CGA pretreatment ameliorated depression-like behavior (SPT, FST, TST, and OFT) and serum biochemical levels (5-HT, DA, IL-6, and TNF-α) in ACTH-induced depression rats. In addition, CGA ameliorated the decrease in fecal microbiota diversity in ACTH-treated rats. In particular, at the genus level, the changes in the relative abundance of some key bacteria such as Desulfovibrionales, Desulfovibrio, Klebsiella, Burkholderiales, and Bifidobacterium were modulated by CGA pretreatment. These results indicated that CGA could modify the gut microbial community structure, which may contribute to its antidepressant effects.