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Gut microbiota: A new target for traditional Chinese medicine in the treatment of depression.
ETHNIC PHARMACOLOGICAL RELEVANCE: The causes of depression are complex. Many factors are involved in its pathogenesis, including the individual's biological and social environment. Although numerous studies have reported that the gut microbiota plays a significant role in depression, drugs that regulate the gut microbiota to treat depression have not yet been comprehensively reviewed. At the same time, more and more attention has been paid to the characteristics of traditional Chinese medicine (TCM) in improving depression by regulating gut microbiota. In ancient times, fecal microbiota transplantation was recorded in TCM for the treatment of severe diseases. There are also records in Chinese ancient books about the use of TCM to adjust gut microbiota to treat diseases, which has opened up a unique research field in TCM. Therefore, this article focuses on the pharmacological effects, targets, and mechanisms of TCM in improving depression by mediating the influence of gut microbiota. AIM OF THIS REVIEW: To summarize the role the gut microbiota plays in depression, highlight potential regulatory targets, and elucidate the anti-depression mechanisms of TCMs through regulation of the gut microbiota. METHODS: A systematic review of 256 clinical trials and pharmaceutical studies published until June 2022 was conducted in eight electronic databases (Web of Science, PubMed, SciFinder, Research Gate, ScienceDirect, Google Scholar, Scopus, and China Knowledge Infrastructure), according to the implemented PRISMA criteria, using the search terms "traditional Chinese medicine," "depression," and "gut microbiota." RESULTS: Numerous studies reported the effects of different gut bacteria on depression and that antidepressants work through the gut microbiota. TCM preparations based on compound Chinese medicine, the Chinese Materia Medica, and major bioactive components exerted antidepressant-like effects by improving levels of neurotransmitters, short-chain fatty acids, brain-derived neurotrophic factor, kynurenine, and cytokines via regulation of the gut microbiota. CONCLUSION: This review summarized the anti-depression effects of TCM on the gut microbiota, providing evidence that TCMs are safe and effective in the treatment of depression and may provide a new therapeutic approach.
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Galactooligosaccharides Attenuate Behavioural, Haematological and Immunological Abnormalities and Influence Gut Microbiota in Rats with Amygdala Hyperactivation Induced by Electrical Stimulation.
The amygdala, especially its central nucleus (CeA), is one of the key brain structures regulating fear, anxiety and stress responses and is also involved in gut microbiota signal processing. Amygdala hyperactivity, as well as microbiota alterations, plays an important role in the pathophysiology of anxiety disorders, depression or post-traumatic stress disorder (PTSD). The present study determines whether 3 weeks of galactooligosaccharide (GOS) supplementation alleviates behavioural, haematological, immunological and gut microbiota disturbances induced by long-term electrical stimulation of the CeA in rats (Stim). The unsupplemented Stim group showed locomotor hyperactivity and higher anxiety (measured with an actometer and the elevated plus maze, respectively), as well as a decrease in white blood cells (WBCs), lymphocytes (LYMs), red blood cells (RBCs) and platelets (PLTs); an elevation of TNFα; a reduction in IL-10 concentration in plasma; and microbiota alterations as compared to the control (Sham) group. GOS supplementation alleviated all these Stim-induced adverse effects or even normalised them to the sham group level. The effect of GOS was comparable to citalopram and even more effective in WBC and PLT normalisation and IL-10 induction. The obtained results indicate the high therapeutic potential of GOS in anxiety and stress-related disorders. GOS supplementation may support conventional therapy or the prevention of PTSD, depression and anxiety disorders.
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Microbiota-Derived SCFAs in Multiple Sclerosis: From Immune Priming to Neurodegeneration.
Multiple sclerosis (MS) is a chronic, immune-mediated neuroinflammatory and neurodegenerative disorder characterized by demyelination, axonal injury, and widespread disruption of central nervous system (CNS) integrity. Clinically heterogeneous and often presenting in young adults-especially women-MS manifests with motor deficits, cognitive impairment, depression, fatigue, sexual and sensory dysfunctions, and autonomic disturbances. Despite advances in immunotherapies, including disease-modifying agents and monoclonal antibodies, current treatments inadequately address progressive neurodegeneration or restore neuronal integrity. Traditional risk factors such as Epstein-Barr virus infection, vitamin D deficiency, smoking, and childhood obesity only partially explain disease onset, reflecting the multifactorial and elusive nature of MS pathogenesis. Recent research has turned attention toward the gut-brain axis, particularly the role of intestinal dysbiosis and microbial metabolites in modulating systemic and CNS inflammation. Among these, short-chain fatty acids (SCFAs)-produced through microbial fermentation of dietary fibres-have emerged as pivotal regulators of immune homeostasis, neuroinflammation, and glial function. Furthermore, MS patients consistently exhibit a depletion of SCFA-producing bacteria, implicating these metabolites development and progression of MS. In the prodromal phase, SCFAs influence gut immune priming and tolerance; in relapsing-remitting MS, they modulate T cell differentiation, cytokine profiles, and remyelination processes; and in progressive MS, they support mitochondrial function, reduce oxidative stress, and influence neuroglial dynamics. While SCFAs show promise as diagnostic biomarkers and adjunctive therapeutic targets, their context-dependent, bidirectional effects necessitate a precision-medicine approach. This review synthesizes current insights into the stage-specific roles of SCFAs across the MS disease continuum. The present work not only elucidates the mechanistic underpinnings of SCFA action in MS but also outlines future directions for microbiota-centred interventions tailored to disease stage and individual microbiome profiles.
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Nano- and micro-polystyrene plastics disturb gut microbiota and intestinal immune system in honeybee.
Micro- (MPs) and nano-plastics (NPs) have become emerging pollutants in the environment. Their wide distribution and capacity as a vector of hazardous materials threaten various organisms. Honeybees have been used as bioindicators for pollutants as their gut microbiota offers advantages for addressing how it alters the host health and exploring the processes of environmental pollutants affecting gut community dynamics. In this study, the effects of plastic particles of different sizes on honeybees' health were investigated. Oral exposure to polystyrene (PS) particles with a diameter of 100 nm significantly decreased the whole-body weight and survival rate of honeybees and induced intestinal dysplasia. As the increase of the feeding time from Day 0 to Day 15, the MPs moved to and accumulated in the rectum, where most bee gut symbionts colonized. Scanning electron microscope observation showed that 100-nm PS particles adhered to the germination pore of pollen, while 1- and 10-μm PS particles were attached by gut bacteria. We found that 100-nm PS treatment decreased the relative abundance of Lactobacillus and Bifidobacterium in the guts. Correspondingly, PS treatment stimulated immune inhibitory genes and depressed genes related to detoxification and energy balance. Furthermore, 100-nm PS treated honeybees became more susceptible to the pathogenic Hafnia alvei, leading to a five-times higher mortality rate. These results indicated the adverse impacts of NPs on honeybees, which extends our knowledge regarding the emerging health risks of plastic debris, especially at the nanoscale.
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Incompatible effects of Panax ginseng and Veratrum nigrum on estrogen decline in rats using metabolomics and gut microbiota.
Panax ginseng (PG) and Veratrum nigrum (VN) are the most representative incompatibility herb pair in traditional Chinese medicine (TCM). This theory is derived from long-term clinical practice and has been applied for thousands of years. However, its mechanism has not yet been clearly investigated. The purpose of this work is to examine the incompatible effects of PG and VN on estrogen decline in rats to better understand the adverse effects of inappropriate herbal combinations using metabolomics and gut microbiota. The ovariectomized rats were administered with PG, VN and their combination decoction decoction intragastrically. After the combination of PG and VN, the improvement of depression-like behavior, neurotransmitter of brain, serum estrogen levels on ovariectomized rats was decreased; the regulation of PG on eight metabolic biomarkers and four intestinal bacteria was reduced by metabolomic and gut microbiota analysis. In addition, the correlation analysis revealed that the above four gut flora showed a relative trend with the significant metabolites of Pantothenic acid, 4, 6-Dihydroxyquinoline, Chenodeoxycholic acid and Caprylic acid. They were involved in tryptophan metabolism, pantothenic acid and coenzyme A biosynthesis, fatty acid biosynthesis and primary bile acid biosynthesis. These results provide further insight into the pathway by which PG and VN combine to reduce the therapeutic effects of estrogen decline. It is helpful to comprehend the incompatible mechanisms of PG and VN.
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Exploring the regulatory mechanism of osteoporosis based on intestinal flora: A review.
Osteoporosis is 1 of the common diseases of bone metabolism in clinic. With the aging of the population in China, osteoporosis is becoming more and more serious, and it has become 1 of the major public health problems. However, traditional therapies, such as calcium therapy and estrogen therapy, can cause serious adverse effects and damage to the body when ingested over a long period of time. Therefore, there is an urgent need to explore alternative therapies with less side effects in clinical practice. Intestinal flora is a hot topic of research in recent years. It has been studied in inflammatory bowel disease, diabetes, depression and so on. Recently, intestinal flora has received increasing attention in the pathways regulating bone metabolism. This paper contains a review of recent studies related to osteoporosis and gut flora in terms of its metabolites, immune, endocrine, and brain-gut axis pathways. The strong association between intestinal flora and bone metabolism suggests, to some extent, that intestinal flora can be a potential target for osteoporosis prevention and treatment, providing new ideas and therapies for the prevention and treatment of osteoporosis.
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Akkermansia muciniphila in neuropsychiatric disorders: friend or foe?
An accumulating body of evidence suggests that the bacterium Akkermansia muciniphila exhibits positive systemic effects on host health, mainly by improving immunological and metabolic functions, and it is therefore regarded as a promising potential probiotic. Recent clinical and preclinical studies have shown that A. muciniphila plays a vital role in a variety of neuropsychiatric disorders by influencing the host brain through the microbiota-gut-brain axis (MGBA). Numerous studies observed that A. muciniphila and its metabolic substances can effectively improve the symptoms of neuropsychiatric disorders by restoring the gut microbiota, reestablishing the integrity of the gut mucosal barrier, regulating host immunity, and modulating gut and neuroinflammation. However, A. muciniphila was also reported to participate in the development of neuropsychiatric disorders by aggravating inflammation and influencing mucus production. Therefore, the exact mechanism of action of A. muciniphila remains much controversial. This review summarizes the proposed roles and mechanisms of A. muciniphila in various neurological and psychiatric disorders such as depression, anxiety, Parkinson's disease, Alzheimer's disease, multiple sclerosis, strokes, and autism spectrum disorders, and provides insights into the potential therapeutic application of A. muciniphila for the treatment of these conditions.
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Elemental iron protects gut microbiota against oxygen-induced dysbiosis.
Gut dysbiosis induced by oxygen and reactive oxygen species may be related to the development of inflammation, resulting in metabolic syndrome and associated-conditions in the gut. Here we show that elemental iron can serve as an antioxidant and reverse the oxygen-induced dysbiosis. Fecal samples from three healthy donors were fermented with elemental iron and/or oxygen. 16S rRNA analysis revealed that elemental iron reversed the oxygen-induced disruption of Shannon index diversity of the gut microbiota.The bacteria lacking enzymatic antioxidant systems also increased after iron treatment. Inter-individual differences, which corresponded to iron oxidation patterns, were observed for the tested donors. Gut bacteria responding to oxygen and iron treatments were identified as guilds, among which, Escherichia-Shigella was promoted by oxygen and depressed by elemental iron, while changes in bacteria such as Bifidobacterium, Blautia, Eubacterium, Ruminococcaceae, Flavonifractor, Oscillibacter, and Lachnospiraceae were reversed by elemental iron after oxygen treatment. Short-chain fatty acid production was inhibited by oxygen and this effect was partially reversed by elemental iron. These results suggested that elemental iron can regulate the oxygen/ROS state and protect the gut microbiota from oxidative stress.
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Impact of outdoor nature-related activities on gut microbiota, fecal serotonin, and perceived stress in preschool children: the Play&Grow randomized controlled trial.
Due to rapid urbanization, children today have fewer opportunities to interact with nature and this may result in a greater risk for developing stress and depression. Outdoor nature-related activities can enhance general well-being. However, the underlying mechanisms are not fully delineated. Here we recruited 54 preschool children to participate in a 10-week structured nature-related "Play&Grow" program. Following the intervention, children were assessed for connectedness to nature and perceived stress levels using validated questionnaires. Moreover, fecal serotonin level and gut microbiota profiles were measured by ELISA and 16S rDNA amplicon sequencing, respectively. Children were significantly more connected to nature after the intervention. Their gut microbiota altered, especially by modulating the abundance of Roseburia and the fecal-serotonin level. Moreover, we also observed a reduction in the overall perceived stress, particularly in the frequency of anger among these children. This study is the first to demonstrate the impact of nature-related activities on gut microbiota, fecal serotonin and psychosocial behaviour of preschool children. However, further mechanistic studies are needed to confirm the functional role of gut microbiota in the association between connectedness to nature and improved psychosocial behavior.
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Defining Dysbiosis in Disorders of Movement and Motivation.
The gut microbiota has emerged as a critical player in shaping and modulating brain function and has been shown to influence numerous behaviors, including anxiety and depression-like behaviors, sociability, and cognition. However, the effects of the gut microbiota on specific disorders associated with thalamo-cortico-basal ganglia circuits, ranging from compulsive behavior and addiction to altered sensation and motor output, are only recently being explored. Wholesale depletion and alteration of gut microbial communities in rodent models of disorders, such as Parkinson's disease, autism, and addiction, robustly affect movement and motivated behavior. A new frontier therefore lies in identifying specific microbial alterations that affect these behaviors and understanding the underlying mechanisms of action. Comparing alterations in gut microbiota across multiple basal-ganglia associated disease states allows for identification of common mechanistic pathways that may interact with distinct environmental and genetic risk factors to produce disease-specific outcomes.