The gut microbiota is a dynamic community of bacteria distributed in the gastroenteric tract and changes in response to diseases, diet, use of antibiotics and probiotics, hygiene status, and other environmental factors. Dysbiosis, a disruption of the normal crosstalk between the host and the microbes, is associated with obesity, diabetes, cancer, and cardiovascular diseases, is linked to a reduction of anti-inflammatory bacteria like Lactobacillus and Roseburia, and to an increase in the growth of proinflammatory species like Ruminococcus gnavus and Bacteroidetes. Some plants possess anticancer properties and various studies have reported that some of these are also able to modulate the gut microbiota. The aim of this work is to evaluate the crucial relationship between medical plants and gut microbiota and the consequences on the onset and progression of cancer. In vivo studies about hematological malignancies showed that beta-glucans tie to endogenous antibeta glucan antibodies and to iC3b, an opsonic fragment of the central complement protein C3, leading to phagocytosis of antibody-targeted neoplastic cells and potentiation of the cytotoxic activity of the innate immune system if administered together with monoclonal antibodies. In conclusion, this review suggests the potential use of medical plants to improve gut dysbiosis and assist in the treatment of cancer. 

The Interplay between Medical Plants and Gut Microbiota in Cancer

Background The standardized treatment of ischemic stroke (IS) with Shuanglu Tongnao Compound Recipe (SLTNCR) combined with Western medicine has improved the life quality and neurological function of patients and achieved a satisfactory clinical effect. However, the underlying mechanisms of SLTNCR in the treatment of IS remain unclear. Methods A rat model of IS was prepared using Longa’s wire bolus method. SLTNCR was administered by gavage with following doses: low dose, 7.16 g·kg−1; middle dose, 14.33 g·kg−1; high dose, 28.66 g·kg−1. The expressions of toll-like receptor 4 (TLR4), tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), IL-6, nuclear factor-κB (NF-κB), etc., brain neuron damage, small intestine structure, and the structure of intestinal flora of rats in the high, medium, and low dose SLTNCR groups as well as the Injury + Clostridium butyricum and Injury + Edaravone groups were detected by 16SrRNA gene sequencing, western blot, hematoxylin-eosin (HE) staining, enzyme-linked immunosorbent assay (ELISA), and polymerase chain reaction (PCR). Results SLTNCR significantly reduced the brain water content, decreased the cerebral infarct size, and improved the neurological deficits, neuronal damage, small bowel tissue damage, and expression of inflammatory factors [B-cell CLL/lymphoma 2 (Bcl-2), BCL2 associated agonist of cell death (Bad), cleaved-caspase-3] in brain tissue. SLTNCR administration significantly inhibited expressions of TLR4, NF-κB, and inhibitor of nuclear factor kappa B (IκB), and decreased phosphorylation levels of NF-κB and IκB in the small intestinal tissues of IS rats. Moreover, SLTNCR also significantly upregulated the expression of intestinal barrier function-related molecules [zona occludens 1 (ZO-1), occludin, claudin-5] and regulated the expression of colonic TLR4, TNF-α, IL-6, and IL-1β. SLTNCR can improve the symptoms of IS rats by improving brain and small intestinal function, particularly by regulating the TLR4/NF-κB signaling pathway, apoptotic proteins, and inflammatory factors in brain tissue. Gut microbiota analysis helped to identify the pharmacological mechanisms underlying the effects of SLTNCR on intestinal bacterial diversity and flora structure in IS rats. Conclusions SLTNCR can alleviate symptoms of IS and the potential mechanism of its effect is to protect brain tissue by suppressing inflammation. SLTNCR can also alter the structure and diversity of the bacterial community in IS.

Zhuang medicine Shuanglu Tongnao Compound Recipe treats stroke by affecting the intestinal flora regulated by the TLR4/NF-κB signaling pathway

The high incidence, mortality, and disability associated with ischemic stroke pose a significant threat to human health. The intestinal microbiota significantly influences the onset, progression, and prognosis of ischemic stroke. Gut flora plays a pivotal role in brain–gut interactions. The reflection of changes in the gut and brain caused by gut microbes facilitates the investigation of early warning biomarkers and potential therapeutic targets for ischemic stroke. In this narrative review of the relationship between gut microbiota and ischemic stroke, we primarily discuss three topics, grounded in real‐world human and animal studies. First, we examined the relationship between ischemic stroke and intestinal microbiota and its metabolites, delineate the overall characteristics of intestinal microbiota dysregulation in ischemic stroke, and assess the potential clinical value, prevailing research controversies, and unique phenomena of intestinal microbiota metabolites such as trimethylamine N‐oxide and short‐chain fatty acids in ischemic stroke. Second, we explored the potential communication pathways between intestinal flora and ischemic stroke based on the brain–gut axis, encompassing metabolic pathways, immune pathways, and neural pathways. Finally, we encapsulated the factors influencing the severity of ischemic stroke via intestinal flora, the pharmacological and nonpharmacological interventions that modulate intestinal flora in treating ischemic stroke, and the current research landscape of intestinal flora in the context of ischemic stroke sequelae.

Role of gut microbiota in ischemic stroke: A narrative review of human and animal studies

The intestinal flora is involved in the maintenance of human health and the development of diseases, and is closely related to the brain. As an essential amino acid, tryptophan (TRP) participates in a variety of physiological functions in the body and affects the growth and health of the human body. TRP catabolites produced by the gut microbiota are important signaling molecules for microbial communities and host-microbe interactions, and play an important role in maintaining health and disease pathogenesis. 

Gut Microbiota and Tryptophan Metabolism in Pathogenesis of Ischemic Stroke: A Potential Role for Food Homologous Plants

Мета роботи. Дослідження впливу гyстого eкстракту з грибів майтаке нa розвиток запальних процесів у білих щурів із доброякісною гіперплазією передміхурової залози, індукованою тестостероном. 
Матеріали і методи. Дослідження проведено на бiлих щурaх-сaмцях, Доброякісну гіперплазію пeредміхурoвої залoзи моделювали шляхoм пiдшкірного ввeдення тeстостерону пропіонату в дoзі 3мг/кг маси тіла тварини протягом 21 дня. Густий екстракт грибів майтаке використовувався для усунення викликаних порушень. Екстракт застосовували перорально щодня протягом трьох тижнів одночасно з тестостероном в дoзі 150 мг/кг мaси тiла твaрини. Як референс-препарат бyло обранo “Простатофіт”, який ввoдили iнтрагастрально за тiєю ж схeмою, щo і дослiджуваний eкстракт в розведенні 1:10 у дозі 1мл/100 г маси тіла щура. На 15 та 22 доби експерименту здійснювали евтаназію щурів із використанням тіопенталу натрію. Протизапальну дію густого екстракту з грибів майтаке оцінювали за наступними біохімічними показниками: кількістю лейкоцитів, величиною швидкості осідання еритроцитів, вмістом С-реактивного протеїну, інтерлейкіну-6, фактора некрозу пухлин-α, тестостерону та дигідротестостерону у сирoватцi кровi тварин. 
Результати й обговорення. Встaновлено експериментально, щo підшкірне ввeдення щyрам тестостерону пропіонату протягом 3 тижнів з метою моделювання доброякісної гіперплазії передміхурової залози призводить до розвитоку запального процесу, що підтверджується достовірним збільшенням кількості лейкоцитів, швидкості осідання еритроцитів, вмісту С-реактивного протеїну, інтерлейкіну-6, фактора некрозу пухлин-α, тестостерону та дигідротестостерону у сироватці крові піддослідних тварин. Застосування густого екстракту мaйтаке в дозi 150 мг/кг тiла твaрини паралельно з тестостероном проявило достовірний позитивний вплив на досліджувані біохімічні показнии в усі терміни експерименту. 
Висновки. Отримані результати підтверджують протизапальні властивості густого екстракту, отриманого з грибів майтаке. Це підтверджує ідею вивчення його потенціалу як простатопротектора та розгляду його інтеграції в комплексний план лікування доброякісної гіперплазії передміхурової залози.

Вплив густого екстракту з грибів майтаке на ознаки запального процесу за умов тестостерон-індукованої доброякісної гiперплазії перeдміхурової залoзи у щyрів

Alcoholic liver damage is caused by long-term drinking, and it further develops into alcoholic liver diseases. In this study, we prepared a probiotic fermentation product of Grifola frondosa total active components (PFGF) by fermentation with Lactobacillus acidophilus, Lactobacillus rhamnosus, and Pediococcus acidilactici. After fermentation, the total sugar and protein content in the PFGF significantly decreased, while the lactic acid level and antioxidant activity of the PFGF increased. Afterward, we investigated the alleviating effect of PFGF on alcoholic liver injury in alcohol-fed mice. The results showed that the PFGF intervention reduced the necrosis of the liver cells, attenuated the inflammation of the liver and intestines, restored the liver function, increased the antioxidant factors of the liver, and maintained the cecum tissue barrier. Additionally, the results of the 16S rRNA sequencing analysis indicated that the PFGF intervention increased the relative abundance of beneficial bacteria, such as Lactobacillus, Ruminococcaceae, Parabacteroids, Parasutterella, and Alistipes, to attenuate intestinal inflammation. These results demonstrate that PFGF can potentially alleviate alcoholic liver damage by restoring the intestinal barrier and regulating the intestinal microflora.

/pdf/probiotics-fermented-grifola-frondosa-total-active-1r9emypl.pdf

Probiotics-Fermented Grifola frondosa Total Active Components: Better Antioxidation and Microflora Regulation for Alleviating Alcoholic Liver Damage in Mice

This study used a metabolomic approach to reveal changes in the levels of metabolic biomarkers and related metabolic pathways before and after Zhuang Yao Shuang Lu Tong Nao granule (YHT) treatment in rats with cerebral ischemia. The neurological deficit scores were significantly higher in the MCAO_R group than in the NC group, indicating that the mice had significantly impaired motor functions. The YHT group had significantly lower scores than the MCAO_R group, suggesting that YHT significantly improved motor function in rats. TTC staining of the brain tissue revealed that YHT significantly reduced the area of cerebral infarction in the treated rats. The MCAO_R group was better separated from the NC rent, sham, and YHT groups via metabolomic PCA. Moreover, there were significant differences in the differential metabolites between the MACO_R and YHT groups. Eighteen common differential metabolites were detected between the MACO_R and NC groups, MACO_R and sham groups, and MACO_R and YHT groups, indicating that YHT significantly increased the levels of various metabolites in the serum of cerebral ischemic stroke (CIS) rats. Moreover, a total of 23 metabolic pathways were obtained. We identified 11 metabolic pathways with the most significant effects in the bubble plots. In conclusion, from a systems biology perspective, this metabolomics-based study showed that YHT could be used to treat ischemic stroke by modulating changes in endogenous metabolites.

/pdf/metabolomics-based-pharmacodynamic-analysis-of-zhuang-yao-11kosr7p.pdf

Metabolomics-Based Pharmacodynamic Analysis of Zhuang Yao Shuang Lu Tong Nao Granules in a Rat Model of Ischemic Cerebral Infarction

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Probiotics-Fermented Grifola frondosa Total Active Components: Better Antioxidation and Microflora Regulation for Alleviating Alcoholic Liver Damage in Mice

Zhuang medicine Shuanglu Tongnao Compound Recipe treats stroke by affecting the intestinal flora regulated by the TLR4/NF-κB signaling pathway

Metabolomics-Based Pharmacodynamic Analysis of Zhuang Yao Shuang Lu Tong Nao Granules in a Rat Model of Ischemic Cerebral Infarction