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Tuberculosis (TB) is one of the leading causes of death in the world, despite being a preventable and curable disease. Irrespective of tremendous advancements in early detection and treatment, this disease still has high mortality rates. This is due to the development of antibiotic resistance, which significantly reduced the efficacy of antibiotics, rendering them useless against this bacterial infection. This, in turn, causes immune system evasion, antibiotic treatment failures, and recurrence of disease in patients. Regarding this, photodynamic inactivation (PDI) may serve as a useful substitute for antibiotic therapy against drug-resistant mycobacteria. This century-old therapy is already being used in cancer treatment, dentistry, and skeletal and cardiovascular diseases, but it is not yet used in tuberculosis treatment. Researchers have previously used PDI to eradicate other members of the genus Mycobacteria in both in vitro and in vivo settings. This suggests PDI can be explored against M. tuberculosis too. The one limitation associated with PDI is the use of chemical photosensitizers, which are fatal to normal tissues and induce side effects. Recent studies suggest herbal photosensitizers are equally potent as chemically synthesized ones. Therefore, herbal photosensitizers could be used to solve the problem because of their less toxicity to healthy tissues and decreased frequency of side effects. This review emphasizes the importance of herbal photosensitizers and their role as anti-tuberculosis drugs in PDI therapy and also presents five potential herbal photosensitizers-curcumin, quercetin, resveratrol, aloe emodin, and phloretin that could be utilized in the clinical development of PDT-mediated tuberculosis therapies. [ABSTRACT FROM AUTHOR]

Introduction: The aim of this study is to examine the physiological effects of emodin on intestinal microorganisms and the liver in the BALb/c mice. Method and Results: Following an 8-week administration of emodin at doses of 25, 50, and 100 mg/kg/day,pathological analyses revealed that emodin significantly reduced the colon length, induced colonic crypt inflammation,diminished the colonic mucus layer,and decreased the fluorescence intensity of colonic tight junction proteins ZO-1 and Occludin. Concurrently, 16S rDNA gene sequencing corroborated that emodin altered the diversity and composition of the intestinal microbiota by increasing the Firmicutes to Bacteroides ratio. Simultaneously, the non-targeted metabolomics analyses exhibited significant alternations in both short chain fatty acids and free fatty acids between the emodin-treated and the normal groups, indicating emodin-induced disturbance in intestinal metabolic disorder. Furthermore, emodin exhibited a significant elevation in LPS levels in colon, serum and liver as well an marked increase in the levels of TC, TG, AST, and ALT in serum. Additionally, histological examination employing by HE and oil-red O staining furtherly verified that the administration of varying doses emodin induced hepatic inflammation and lipid accumulation. Whereas qRT-PCR and Western blot analyses demonstrated that the administering of varying doses of emodin upregulated the mRNA levels of TNF-α, IL-1β, IL-6, and IL-18 as well as the expression of TLR4, Myd88, and P-65. Following the combined administration of probiotics, the high-dose emodin did not significantly influence ALT and AST levels in mice. However, the faeces of the high-dose emodin transplanted in mice and induced a significant increase in AST levels and in the relative abundance of Firmicutes and Proteobacteria. Discussion: These findings further corroborate that emodin induces liver injury via the intestinal dysfunction. These findings suggested that emodin may disrupt intestinal microbiota and resulted in significant alternations in endogenous metabolites in mice, thereby facilitating the entry of LPS and FFAs into the liver, potentially leading to hepatic injury. [ABSTRACT FROM AUTHOR]

Lung cancer is one of the most common malignant tumors in the world, with high incidence rate and mortality. Monocarboxylate transporter (MCT) 1 has been found to be widely expressed in various tumors and plays a crucial role in regulating energy metabolism. Emodin, as an important traditional Chinese medicine in China, has been reported to inhibit the progression of lung cancer. However, its potential mechanism has not been fully elucidated. The effects of emodin and MCT1 inhibitor AZD3965 on the proliferation, migration, and invasion of lung cancer cells were detected using cell counting kit-8 (CCK-8) assay, wound-healing assay, and transwell small chamber assay. The content of glucose, lactate, and pyruvate in the cell culture medium was detected using a glucose, lactate, and pyruvate detection kit, and also detected protein expression using western blotting. In addition, to investigate the effects of emodin and AZD3965 on lung cancer in vivo, we constructed nude mice subcutaneous transplant tumor model by subcutaneous injection of lung cancer cells. The results showed that emodin and AZD3965 could inhibit the proliferation, migration, and invasion of lung cancer cells. At the same time, they could inhibit the expression of MCT1 in lung cancer cells and promote the release of lactate, but did not affect the content of glucose and pyruvate. In vivo experiments had shown that emodin and AZD3965 could effectively inhibit the growth of lung cancer and inhibit the expression of MCT1. All in all, our data suggested that emodin inhibited the proliferation, migration, and invasion of lung cancer cells, possibly by inhibiting MCT1, providing important theoretical basis for elucidating the mechanism of emodin in treating lung cancer.Highlights: Emodin could inhibit proliferation, migration, and invasion of lung cancer cells. Emodin could inhibit the expression of monocarboxylate transporter 1, a key mediator of lactate shuttle. Emodin could inhibit the expression of oncogenes in lung cancer cells. Emodin and AZD3965 could inhibit the growth of subcutaneous transplanted tumors in nude mice. [ABSTRACT FROM AUTHOR]

Yinchenhao decoction (YCHD) is widely used in the treatment of damp-heat syndrome of chronic hepatitis B (CHB), but it remains unclear about the active compounds in YCHD and its potential mechanism for treating CHB. The purpose of this work is to evaluate the clinical efficacy of YCHD combined with nucleoside analogues (NAs) for the treatment of CHB. Besides, based on the exact clinical efficacy, we combined serum metabolomics and network pharmacology to screen differential metabolites and related pathways regulated by YCHD to investigate the possible mechanism for treating CHB. It revealed that NAs plus YCHD could significantly improve alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, increase HBV-DNA negative rate (P <0.05), reduce the levels of inflammatory factors and LSM (both P <0.05), regulate lipids (P <0.05), and improve the symptoms of traditional Chinese medicine (TCM) (P <0.05) in CHB patients. YCHD was relatively safe. It showed 30 active compounds including chlorogenic acid, geniposide, emodin, quercetin, kaempferol, β-sitosterol and aloe emodin, and 115 key targets which were related to the regulation of lipids and reduction of oxidative stress related to the effect of YCHD in CHB in the network pharmacology analysis. We found 9 core targets and 4 key metabolites according to metabolomics, which were partly consistent with the network pharmacology findings. It proved that network pharmacology combined with metabolomics can well explain the "multi-component-multi-target" mechanism of complex TCM. [Display omitted] • Based on clinical study, the efficacy of combination drugs is assessed, new treatments are explored. • Advancing the application of network pharmacology and metabolomics, uncovering the multi-target mechanisms of YCHD combined with NAs in treating CHB. [ABSTRACT FROM AUTHOR]