Intestinal anti-inflammatory effects of fuzi-ganjiang herb pair against DSS-induced ulcerative colitis in mice

Huang, Chensihan; Dong, Junli; Jin, Xiaoqi; Ma, Haoran; Zhang, Dan; Fu-qian, Wang; Cheng, Lü; Yan, Feng; Xiong, Xin; Jiang, Jie; Hu, Lei; Lei, M.; Wu, Bin; Zhang, Geng

doi:10.1016/j.jep.2020.112951

Cited by 29 publications

(26 citation statements)

References 33 publications

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“…Therefore, the mucosal barrier gets broken. Then, the immune inflammation in lamina propria is induced by the invasion and destruction of harmful dietary antigens and pathogens, triggering oxidative stress ( Sands, 2015 ; Huang et al, 2020 ; Ke, 2020 ; Zhao et al, 2020 ). Oxidative stress and immune inflammation affect each other and aggravate the pathological process of UC together.…”

Section: Discussionmentioning

confidence: 99%

Construction of a “Bacteria-Metabolites” Co-Expression Network to Clarify the Anti–Ulcerative Colitis Effect of Flavonoids of Sophora flavescens Aiton by Regulating the “Host–Microbe” Interaction

Shao

Gao

et al. 2021

Front. Pharmacol.

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Ulcerative colitis (UC) is considered an immune disease, which is related to the dysbiosis of intestinal microbiota and disorders of the host immune system and metabolism. Sophora flavescens Aiton has been used for the clinical treatment of UC in China and East Asia for thousands of years. It has many traditional prescriptions and modern preparations, and its curative effects are definite. We are the first to report that the flavonoids in Sophora flavescens (S. flavescens) Aiton EtOAc extract (SFE) could potentially attenuate the dextran sodium sulfate–induced UC in mice, which changed the current understanding of considering alkaloids as the only anti-UC pharmacological substances of S. flavescens Aiton. Based on the 16S rRNA gene sequencing and metabolomic analysis, it was found that the anti-UC effects of SFE were due to the regulation of gut microbiota, reversing the abnormal metabolisms, and regulation of the short-chain fatty acids synthesis. Notably, according to the interaction networks of specific bacteria and “bacteria and metabolites” co-expression network, the SFE could enrich the abundance of the commensal bacterium Lactobacillus, Roseburia, norank_f__Muribaculaceae, Anaerotruncus, Candidatus_Saccharimona, and Parasutterella, which are proposed as potentially beneficial bacteria, thereby playing vital roles in the treatment of UC.

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Section: Discussionmentioning

confidence: 99%

Construction of a “Bacteria-Metabolites” Co-Expression Network to Clarify the Anti–Ulcerative Colitis Effect of Flavonoids of Sophora flavescens Aiton by Regulating the “Host–Microbe” Interaction

Shao

Gao

et al. 2021

Front. Pharmacol.

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“…Tissue damage was scored as the following criteria [ 42 ]: 0, no damage; 1, lymphoepithelial lesions; 2, focal ulceration or surface mucosal erosion; 3, broad mucosal damage involving deeper structures of the intestinal wall. Inflammatory cell infiltration score was evaluated according to the criteria below [ 42 ]: 0, few inflammatory cells in the lamina propria; 1, increased infiltration of inflammatory cells into the lamina propria; 2, the group of inflammatory cells infiltrating into the submucosa; 3, transmural infiltration of inflammatory cells. Then, the histological score was determined by combining the scores of tissue damage and inflammatory cell infiltration.…”

Section: Methodsmentioning

confidence: 99%

Fecal microbiota transplantation protects rotenone-induced Parkinson’s disease mice via suppressing inflammation mediated by the lipopolysaccharide-TLR4 signaling pathway through the microbiota-gut-brain axis

et al. 2021

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Background Parkinson’s disease (PD) is a prevalent neurodegenerative disorder, displaying not only well-known motor deficits but also gastrointestinal dysfunctions. Consistently, it has been increasingly evident that gut microbiota affects the communication between the gut and the brain in PD pathogenesis, known as the microbiota-gut-brain axis. As an approach to re-establishing a normal microbiota community, fecal microbiota transplantation (FMT) has exerted beneficial effects on PD in recent studies. Here, in this study, we established a chronic rotenone-induced PD mouse model to evaluate the protective effects of FMT treatment on PD and to explore the underlying mechanisms, which also proves the involvement of gut microbiota dysbiosis in PD pathogenesis via the microbiota-gut-brain axis. Results We demonstrated that gut microbiota dysbiosis induced by rotenone administration caused gastrointestinal function impairment and poor behavioral performances in the PD mice. Moreover, 16S RNA sequencing identified the increase of bacterial genera Akkermansia and Desulfovibrio in fecal samples of rotenone-induced mice. By contrast, FMT treatment remarkably restored the gut microbial community, thus ameliorating the gastrointestinal dysfunctions and the motor deficits of the PD mice. Further experiments revealed that FMT administration alleviated intestinal inflammation and barrier destruction, thus reducing the levels of systemic inflammation. Subsequently, FMT treatment attenuated blood-brain barrier (BBB) impairment and suppressed neuroinflammation in the substantia nigra (SN), which further decreased the damage of dopaminergic neurons. Additional mechanistic investigation discovered that FMT treatment reduced lipopolysaccharide (LPS) levels in the colon, the serum, and the SN, thereafter suppressing the TLR4/MyD88/NF-κB signaling pathway and its downstream pro-inflammatory products both in the SN and the colon. Conclusions Our current study demonstrates that FMT treatment can correct the gut microbiota dysbiosis and ameliorate the rotenone-induced PD mouse model, in which suppression of the inflammation mediated by the LPS-TLR4 signaling pathway both in the gut and the brain possibly plays a significant role. Further, we prove that rotenone-induced microbiota dysbiosis is involved in the genesis of PD via the microbiota-gut-brain axis.

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“…In traditional Chinese medicine, herb couples can provide the optimal efficacy of the formulae. Fuzi-Ganjiang (FG) is a classic herb couple among traditional medicine formulae for treating shock, heart failure, diarrhea, and other diseases characterized by Yang deficiency (Huang et al, 2020a). The theory of traditional Chinese medicine believes that Ganjiang can enhance the efficacy of Fuzi, namely, "Fuzi would not exert its heating efficacy without Ganjiang," and multiple research studies have also found that Ganjiang and Fuzi used together can significantly heighten the pharmacological activity of those two used alone (Wen-Wen et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…The theory of traditional Chinese medicine believes that Ganjiang can enhance the efficacy of Fuzi, namely, "Fuzi would not exert its heating efficacy without Ganjiang," and multiple research studies have also found that Ganjiang and Fuzi used together can significantly heighten the pharmacological activity of those two used alone (Wen-Wen et al, 2013). Furthermore, the addition of Ganjiang could reduce the dissolution of Fuzi alkaloids, especially the acute toxic diester alkaloids, and the addition of Fuzi increased the content of gingerol compared with that in a decoction of Ganjiang alone (Huang et al, 2020a). Through the optimized UPLC-Q-TOF-MS E technique, a total of 49 compounds in the FG extraction were discovered, including 30 compounds from Fuzi (Table 1 and Figure 1) and 19 compounds from Ganjiang (Table 2 and Figure 2).…”

Section: Discussionmentioning

confidence: 99%

The Anti-Neuroinflammatory Effect of Fuzi and Ganjiang Extraction on LPS-Induced BV2 Microglia and Its Intervention Function on Depression-Like Behavior of Cancer-Related Fatigue Model Mice

Yang

Chen

et al. 2021

Front. Pharmacol.

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The Chinese herb couple Fuzi and Ganjiang (FG) has been a classic combination of traditional Chinese medicine that is commonly used clinically in China for nearly 2000 years. Traditional Chinese medicine suggests that FG can treat various ailments, including heart failure, fatigue, gastrointestinal upset, and depression. Neuroinflammation is one of the main pathogenesis of many neurodegenerative diseases in which microglia cells play a critical role in the occurrence and development of neuroinflammation. FG has been clinically proven to have an efficient therapeutic effect on depression and other neurological disorders, but its mechanism remains unknown. Cancer-related fatigue (CRF) is a serious threat to the quality of life of cancer patients and is characterized by both physical and psychological fatigue. Recent studies have found that neuroinflammation is a key inducement leading to the occurrence and development of CRF. Traditional Chinese medicine theory believes that extreme fatigue and depressive symptoms of CRF are related to Yang deficiency, and the application of Yang tonic drugs such as Fuzi and Ganjiang can relieve CRF symptoms, but the underlying mechanisms remain unknown. In order to define whether FG can inhibit CRF depression-like behavior by suppressing neuroinflammation, we conducted a series of experimental studies in vitro and in vivo. According to the UPLC-Q-TOF/MSE results, we speculated that there were 49 compounds in the FG extraction, among which 30 compounds were derived from Fuzi and 19 compounds were derived from Ganjiang. Our research data showed that FG can effectively reduce the production of pro-inflammatory mediators IL-6, TNF-α, ROS, NO, and PGE2 and suppress the expression of iNOS and COX2, which were related to the inhibition of NF-κB/activation of Nrf2/HO-1 signaling pathways. In addition, our research results revealed that FG can improve the depression-like behavior performance of CRF model mice in the tail suspension test, open field test, elevated plus maze test, and forced swimming test, which were associated with the inhibition of the expression of inflammatory mediators iNOS and COX2 in the prefrontal cortex and hippocampus of CRF model mice. Those research results suggested that FG has a satisfactory effect on depression-like behavior of CRF, which was related to the inhibition of neuroinflammation.

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Intestinal anti-inflammatory effects of fuzi-ganjiang herb pair against DSS-induced ulcerative colitis in mice

Cited by 29 publications

References 33 publications

Construction of a “Bacteria-Metabolites” Co-Expression Network to Clarify the Anti–Ulcerative Colitis Effect of Flavonoids of Sophora flavescens Aiton by Regulating the “Host–Microbe” Interaction

Construction of a “Bacteria-Metabolites” Co-Expression Network to Clarify the Anti–Ulcerative Colitis Effect of Flavonoids of Sophora flavescens Aiton by Regulating the “Host–Microbe” Interaction

Fecal microbiota transplantation protects rotenone-induced Parkinson’s disease mice via suppressing inflammation mediated by the lipopolysaccharide-TLR4 signaling pathway through the microbiota-gut-brain axis

The Anti-Neuroinflammatory Effect of Fuzi and Ganjiang Extraction on LPS-Induced BV2 Microglia and Its Intervention Function on Depression-Like Behavior of Cancer-Related Fatigue Model Mice

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