Frontiers in Pharmacology
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2024
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IF 4.4
Zhixiang Zhu,Yuanjing Zou,Ling Ou,Meiyun Chen,Yujiang Pang,Hui Li,Yajie Hao,Bingmei Su,Yuqian Lai,Liping Zhang,Junwei Jia,Ruixia Wei,Guimin Zhang,Meicun Yao,Zhong Feng
Background: Triphala, is a composite of three individual botanical drugs: Terminalia chebula, Terminalia bellirica, and Emblica officinalis. It exhibits properties such as heatclearing, anti-inflammatory, anti-fatigue, antioxidant, and antibacterial effects,making it extensively utilized in India and Tibet. It has been found to exhibitinhibitory effects on Helicobacter pylori (H. pylori); however, further comprehensive research is still needed to elucidate its specific antibacterial mechanism. The present study investigates the in vitro antibacterial activity and antibacterial mechanism of Triphala against H. pylori.Methods: Ours research investigates the in vitro inhibitory activity of Triphala on multiple standard and clinical strains using microdilution broth method, time-kill curve, time-bactericidal curve and scanning electron microscopy (SEM). Furthermore, the antibacterial mechanism of Triphala is further explored through experiments on urease activity, biofilm formation, anti-adhesion properties, virulence actor assays using RT-qPCR and Western Blotting techniques.Results: The research findings indicate that Triphala exhibits a minimum inhibitory concentration of 80–320 μg/mL against both standard and clinical strains of H. pylori. Triphala exerts its anti-H. pylori effect by perturbing the microstructure of H. pylori, downregulating adhesion-associated genes (alpA, alpB, babA), urease-related genes (ureA, ureB, ureE, ureF), and flagellar genes (flaA, flaB); inhibiting bacterial adhesion, biofilm formation, urease activity as well as CagA protein expression.Discussion: These findings suggest that Triphala exerts inhibitory effects on H. pylori activity through multiple mechanisms, underscoring its potential as a new drug for the prevention and treatment of H. pylori infection.
研究领域:
药理学
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微生物学
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传统医学
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DOI
PubMed
高影响因子
Biomed Research International
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2021
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IF 3.411
Wanchen Ning,Simin Li,Jokyab Tsering,Yihong Ma,Honghong Li,Yuezhu Ma,Anthony Chukwunonso Ogbuehi,Hongying Pan,Hanluo Li,Shaonan Hu,Xiangqiong Liu,Yupei Deng,Jianlin Zhang,Xianda Hu
Background. Oxidative stress is implicated in the progression of many neurological diseases, which could be induced by various chemicals, such as hydrogen peroxide (H2O2) and acrylamide. Triphala is a well-recognized Ayurvedic medicine that possesses different therapeutic properties (e.g., antihistamine, antioxidant, anticancer, anti-inflammatory, antibacterial, and anticariogenic effects). However, little information is available regarding the neuroprotective effect of Triphala on oxidative stress. Materials and Methods. An in vitro H2O2-induced SH-SY5Y cell model and an in vivo acrylamide-induced zebrafish model were established. Cell viability, apoptosis, and proliferation were examined by MTT assay, ELISA, and flow cytometric analysis, respectively. The molecular mechanism underlying the antioxidant activity of Triphala against H2O2 was investigated dose dependently by Western blotting. The in vivo neuroprotective effect of Triphala on acrylamide-induced oxidative injury in Danio rerio was determined using immunofluorescence staining. Results. The results indicated that Triphala plays a neuroprotective role against H2O2 toxicity in inhibiting cell apoptosis and promoting cell proliferation. Furthermore, Triphala pretreatment suppressed the phosphorylation of the mitogen-activated protein kinase (MARK) signal pathway (p-Erk1/2, p-JNK1/2, and p-p38), whereas it restored the activities of antioxidant enzymes (superoxide dismutase 1 (SOD1) and catalase) in the H2O2-treated SH-SY5Y cells. Consistently, similar protective effects of Triphala were observed in declining neuroapoptosis and scavenging free radicals in the zebrafish central neural system, possessing a critical neuroprotective property against acrylamide-induced oxidative stress. Conclusion. In summary, Triphala is a promising neuroprotective agent against oxidative stress in SH-SY5Y cells and zebrafishes with significant antiapoptosis and antioxidant activities.
研究领域:
神经科学
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药理学
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毒理学
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阿育吠陀医学
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DOI
PubMed
高影响因子
PHYTOMEDICINE
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2026
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IF 11.3
Cong Liu,Huan Zhang,Huihui Zhang,Yi Zhao,Chen Wu,Qinxiong Lin,Yubin Luo,Liangkai Wei,Jianqiu Chen,Xinyu Rao,Siyi Xiong,Hanmeng Shen,Shuyan Hong,Zhaohua Shi,Shijin Yin,Zhou Lan,Lvyi Chen
Chebulic acid, gallic acid, and corilagin predominated among the seven quantified analytical markers in the TRP aqueous extract. • TRP acts as a potent microbiota modulator to ameliorate renal injury. • The lysophospholipid-TLR4 axis serves as one of the pathological drivers of HUA-associated chronic renal injury. • LPC 16:0 and LPC 18:1 trigger renal inflammation by activating the TLR4 pathway. Background Hyperuricemia (HUA) is a metabolic disorder with an escalating global prevalence, and its progression to HUA-associated nephropathy represents an important contributor to chronic kidney injury. Emerging evidence highlights a bidirectional relationship between uric acid and lipid metabolism, with dyslipidemia contributing to the pathological progression of HUA-related complications. Triphala (TRP), a classic Tibetan herbal formula with broad metabolic regulatory properties, was selected as a potential intervention for the complex metabolic disturbances associated with HUA. However, its therapeutic efficacy and the precise molecular mechanisms underlying its effects in HUA remain to be fully elucidated. Purpose This study aimed to investigate the protective effects of TRP on hyperuricemia-associated nephropathy and to elucidate the underlying mechanisms. Methods High-performance liquid chromatography (HPLC) was first employed to identify and quantify seven representative constituents in the TRP aqueous extract. To evaluate the efficacy of TRP, an HUA mouse model was established through the combined administration of intraperitoneal potassium oxonate injections and a yeast-containing diet. A multi-omics strategy integrating 16S rRNA sequencing, metabolomics and lipidomics elucidated TRP's impact on the gut microbiota and host metabolism. Critically, fecal microbiota transplantation (FMT), TLR4 blockade experiments, and in vitro assays were employed to evaluate the contribution of TRP-modulated microbiota and the LPC-TLR4 pathway to the protective effects of TRP. Results HPLC identified chebulic acid, gallic acid, and corilagin as the major representative constituents of TRP aqueous extract. TRP dose-dependently reduced serum uric acid, improved renal function by lowering serum creatinine (Cr) and blood urea nitrogen (BUN) levels, increased the fractional excretion of uric acid (FEUA), and alleviated tubular injury and fibrosis. These improvements were accompanied by normalized urate transporters (downregulated URAT1/GLUT9; restored OAT1/OAT3) and suppressed renal inflammatory cytokines. Multi-omics analysis revealed that TRP reversed HUA-induced dysbiosis by suppressing opportunistic pathogens (e.g., Parasutterella, Allobaculum ) and enriching beneficial genera (e.g., Bifidobacterium, Akkermansia ), specifically reducing pro-inflammatory LPC (e.g., LPC16:0, LPC18:1). TRP and FMT effectively inhibited the TLR4/MyD88/NF-κB signaling axis and reduced LPC accumulation within the kidney. In vitro experiments validated that these specific LPC directly trigger TLR4 expression and TNF-α release, confirming the potential role of the microbiota-driven lysophospholipid-TLR4 pathway in HUA-associated chronic renal inflammation. Conclusion TRP ameliorates HUA and renal inflammation by remodeling the gut microbiota to suppress the aberrant accumulation of pro-inflammatory lysophospholipids, thereby deactivating the TLR4-mediated inflammatory cascade. These findings establish the gut microbiota-glycerophospholipid metabolism-renal inflammation axis as a potential therapeutic target and validate TRP as a relevant strategy for targeting the gut microbiome to treat systemic metabolic disease. Download: Download high-res image (331KB) Download: Download full-size image
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