Introduction The global use of Chinese herbal medicines (CHMs) alongside pharmaceutical drugs has increased the need for systematic assessment of herb–drug interactions (HDIs) to support safe integrative practice. However, existing databases show limited CHM coverage, inconsistent evidence grading, and poor clinical interpretability. This review describes the systematic development of evidence-based Chinese HDI monographs for IMgateway (https://www.imgateway.net), using dual-language English and Chinese evidence, predefined evidence-level classification, causality assessment, and interaction likelihood grading to support clinically interpretable decision-making. Methods A structured three-phase methodology was applied to evaluate 200 commonly used Chinese herbs. Comprehensive searches were conducted across English- and Chinese-language databases. Standardized criteria were developed to assess interaction likelihood, strength of evidence, mechanistic plausibility, causality, and potential clinical relevance across different levels of available evidence. Results A total of 497 peer-reviewed articles were included, from which 595 HDI monographs were developed. The included evidence comprised clinical studies, including randomized controlled trials (RCTs) and human case reports, and preclinical studies, including in vitro and in vivo investigations. Based on monograph classification, 241 monographs were derived from RCTs, 27 from human case reports, and 327 from preclinical studies. Interactions were categorized according to evidence level and assigned likelihood classifications. Seven HDIs were categorized as “avoid combination,” and 114 as “caution,” highlighting clinically significant safety concerns. In addition, 295 HDIs were classified as potentially beneficial, 73 as unlikely, and 106 as unresolved. Evidence strength was further classified as well-established (n = 28), good (n = 76), limited (n = 395), and unknown (n = 96). Conclusion By integrating dual-language evidence and standardized grading criteria, the database enhances prescribing safety, supports patient counselling, and strengthens pharmacovigilance in integrative healthcare settings. Continuous updates and prospective validation will further improve its clinical applicability.

Amyotrophic lateral sclerosis (ALS) is a debilitating and fatal neurodegenerative disease characterised by the progressive loss of motor functions affecting both upper and lower motor neurons. Although considered multifactorial with an unclear aetiology, it is believed that the interplay between genetic and environmental factors, with neuroinflammation playing a key role in disease progression, contributes to its development. There is currently no effective treatment for ALS.Curcumin has been recently highlighted for its potential therapeutic role in treating neurodegenerative diseases. Curcumin phospholipids, a highly bioavailable form of curcumin that allow the curcumin to be absorbed into the bloodstream more effectively than standard curcumin extracts, is considered as a natural cytokine-suppressive anti-inflammatory compound (CSAID) that is well-known for its therapeutic properties and is considered safe for humans and rodents at low to moderate concentrations. In this study, we investigated whether a long-term feeding regimen incorporating curcuminoids phospholipids-enriched diet early in disease progression could mitigate motor deficits and affect the lifespan of the SOD1 mouse model of familial ALS (fALS).Our results indicate sex-differences regarding the effect of curcumin supplementation on motor deficits and anxiety-like behaviour. While long-term feeding with curcuminoids phospholipids enriched diet had a complex effect on SOD1 female mice expressed as reduced anxiety like behaviour and motor deficits at the walking beam test, it had no effect on SOD1 male mice. Moreover, curcuminoids supplementation had a limited effect on disease onset and progression in SOD1 mice model for fALS.

Seven new arylalkenyl α,β-unsaturated-δ-lactones, triplinones I-O (1-7), were isolated from the leaves of the Australian rainforest plant Cryptocarya triplinervis B. Hyland (Lauraceae). The chemical structures of these compounds were established by NMR spectroscopic data analysis, while their relative and absolute configurations were established using a combination of Mosher ester analysis utilizing both Riguera's and Kishi's methods and CD experiments. Compounds 2 and 4 were identified as epimers, where the relative stereochemistry of the 1,3-diol moiety in both structures was first confirmed by Kishi's method, followed by their absolute configuration determination using Riguera's method. Compounds 1-7 exhibited good inhibitory activities toward nitric oxide (NO) production in lipopolysaccharide (LPS) and interferon (IFN)-γ-induced RAW 264.7 macrophages, in particular compounds 6, 2, and 4, with IC50 values of 2.1 ± 1.4, 8.5 ± 0.6, and 8.5 ± 0.7 μM, respectively.

Inflammation contributes to the progression of numerous chronic diseases, and plants are a rich source of bioactive secondary metabolites. In this study, bioassay-guided isolation of the previously unexplored Australian native plant Beyeria viscosa (Labill.) Miq. yielded eleven known compounds (1-11). The chemical structures of these compounds were identified by detailed spectroscopic data analysis, and definitive structural confirmation was established using single-crystal X-ray crystallography for fritillebic acid (8) and herbacetin 3,7,8-trimethyl ether (5) for the first time. All compounds were first screened for nitric oxide (NO) inhibitory activity and cytotoxicity in lipopolysaccharide (LPS) and interferon (IFN)-γ-stimulated RAW 264.7 macrophages, and the active NO inhibitors were further assessed for tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) inhibition. Notably, compounds 5, 8, and 10 were evaluated for NO inhibitory activity for the first time, with compound 8 being the most potent (IC50 = 8.8 ± 1.3 μM), compound 10 showing moderate potency (IC50 = 12.2 ± 8.8 μM), and compound 5 being inactive. Among all tested compounds, fritillebic acid (8) emerged as the most active constituent, showing strong NO inhibition and moderate suppression of TNF-α and IL-6 production; therefore, it was further assessed in LPS-stimulated N-11 microglial cells, where it retained NO inhibitory activity (IC50 = 12.3 ± 0.5 μM) with a favorable activity-cytotoxicity profile (LC50 = 107.9 ± 1.9 μM). Consistent with the promising activity, molecular docking of compound 8 showed strong receptor-binding affinity with selected inflammation-related targets. Moreover, preliminary structure-activity relationship analysis of all isolated compounds suggested that substitution and oxygenation patterns may influence NO inhibitory potency. Overall, these findings identify fritillebic acid as the major anti-inflammatory lead from B. viscosa and highlight Australian native plants as a source of bioactive secondary metabolites.

Background/Objectives: Oxidative stress is a well-established driver of neuronal dysfunction and a shared pathological mechanism across neurodegenerative diseases. Pharmacological activation of the Nrf2/ARE pathway is a validated strategy to counteract oxidative damage, as demonstrated by the clinical approval of dimethyl fumarate (DMF) and monomethyl fumarate (MMF) for relapsing forms of multiple sclerosis. These electrophilic compounds activate Nrf2 via covalent Keap1 modification. Cynara scolymus L. structurally related electrophilic metabolites; however, their contribution to Nrf2 activation remains undefined. This study aimed to identify and characterize the constituents responsible for Nrf2 activation and benchmark their potency against DMF and MMF. Methods: Bioactivity-guided fractionation combining Soxhlet extraction, Nrf2/ARE luciferase reporter screening, semi-preparative HPLC, and spectroscopic identification was employed. Functional validation included extracellular thiol quantification, H₂O₂ cytoprotection assays, and western blot analysis of heme oxygenase-1 (HO-1). Results: The dichloromethane extract exhibited the highest Nrf2-inducing activity (54.4 - fold). Fractionation yielded five guaianolide sesquiterpene lactones (1-5), four of which were active. The α-methylene-γ-lactone moiety was essential for activity. Aguerin B (3) exhibited the highest activity (39.14 ± 11.13-fold), while TBA analysis identified cynaropicrin (2) as the dominant extract-level contributor (62.9% of total activity). Notably, aguerin B and cynaropicrin (2) induced greater activation than DMF and MMF in Nrf2/ARE reporter assay. Downstream pathway activation was confirmed by concentration- and time-dependent HO-1 upregulation, elevated extracellular glutathione and CysGly levels, and significant protection against H₂O₂-induced cytotoxicity without intrinsic toxicity. Conclusions: Guaianolide sesquiterpene lactones are the primary mediators of Nrf2 activation in C. scolymus. Cynaropicrin (2) exhibited superior in vitro potency over fumarates, supporting its relevance for further pharmacological investigation.

Background/Objectives: Oxidative and electrophilic stress-response pathways contribute to cellular resilience across various chronic diseases, including neurodegenerative, hepatic, and metabolic disorders. Pharmacological activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway is a validated strategy to counteract oxidative damage, as evidenced by the clinical approval of dimethyl fumarate (DMF) and monomethyl fumarate (MMF) for relapsing forms of multiple sclerosis; both electrophilic compounds activate Nrf2 via covalent Keap1 (Kelch-like ECH-associated protein 1) modification. Cynara scolymus L. contains structurally related electrophilic metabolites; however, their contribution to Nrf2-associated signaling remains undefined. This study aimed to identify and characterize the constituents responsible for Nrf2-inducing activity and benchmark their potency against DMF and MMF. Methods: Bioactivity-guided fractionation combining Soxhlet extraction, Nrf2/ARE luciferase reporter screening, semi-preparative HPLC, and spectroscopic identification was employed. Functional validation included extracellular thiol quantification, H2O2 cytoprotection assays, and Western blot analysis of heme oxygenase-1 (HO-1). Results: The dichloromethane extract exhibited the highest Nrf2-inducing activity (54.4-fold). Fractionation yielded five guaianolide sesquiterpene lactones (1–5), four of which were active. The α-methylene-γ-lactone moiety was essential for activity. Aguerin B (3) exhibited the highest activity (39.14 ± 11.13-fold), while TBA analysis identified cynaropicrin (2) as the dominant extract-level contributor (62.9% of total activity). Notably, aguerin B (3) and cynaropicrin (2) induced greater reporter activity than DMF and MMF. Downstream pathway induction was confirmed by concentration- and time-dependent HO-1 upregulation, elevated extracellular glutathione and cysteinylglycine levels, and significant protection against H2O2-induced cytotoxicity without intrinsic toxicity. Conclusions: Guaianolide sesquiterpene lactones are the primary mediators of Nrf2-associated antioxidant signaling in C. scolymus. Cynaropicrin (2) exhibited stronger in vitro ARE-reporter induction than fumarates, supporting its relevance for further pharmacological investigation.

Background/Objectives: Curcumin, the principal bioactive component of Curcuma longa, is known for its anti-inflammatory, antioxidant, and neuroprotective properties. Despite its therapeutic potential, curcumin exhibits poor oral bioavailability due to low solubility, rapid metabolism, and limited gastrointestinal absorption. Various delivery systems have been developed to overcome these limitations. This study aimed to evaluate and compare the pharmacokinetic profile of AQUATURM®, a novel, water-soluble curcumin formulation, with that of a widely available commercial curcumin supplement. Methods: A randomized, double-blind, two-period crossover study was conducted in 12 healthy adult participants (6 male, 6 female; aged 20–45 years). Each participant received a single oral dose of either AQUATURM® or the comparator product, followed by a 7-day washout period before receiving the alternate treatment. Blood samples were collected at multiple time points over a 12-h period post-dosing. Plasma curcumin concentrations were quantified using ultra-performance liquid chromatography with tandem mass spectrometry (UPLC-MS/MS). Results: AQUATURM® achieved a significantly higher systemic exposure compared to the comparator, with a more than 7-fold increase in area under the curve (AUC0–12h) and higher peak plasma concentrations (Cmax). AQUATURM® also maintained detectable curcumin levels for the full 12-h observation period, whereas levels from the comparator fell below quantification limits in most participants after 4 h. Conclusions: AQUATURM® significantly enhances curcumin bioavailability in humans compared to a standard curcumin formulation. These pharmacokinetic improvements support its potential for greater clinical efficacy and warrant further evaluation in therapeutic setting

Lymphoma continues to pose a significant global health burden, highlighting the urgent need for novel therapeutic strategies. Recent advances in microbiome research have identified gut-microbiota-derived metabolites, or postbiotics, as promising candidates in cancer therapy. This study investigates the antiproliferative and mechanistic effects of two postbiotics, Nisin (N) and Urolithin B (UB), individually and in combination, against the human lymphoma cell line HKB-11. Moreover, this study evaluated cytotoxic efficacy and underlying molecular pathways using a comprehensive experimental approach, including the Alamar Blue assay, combination index (CI) analysis, flow cytometry, reactive oxygen species (ROS) quantification, and bottom-up proteomics. N and UB displayed notable antiproliferative effects, with IC50 values of 1467 µM and 87.56 µM, respectively. Importantly, their combination at a 4:6 ratio demonstrated strong synergy (CI = 0.09 at IC95), significantly enhancing apoptosis (p ≤ 0.0001) and modulating oxidative stress. Proteomic profiling revealed significant regulation of key proteins related to lipid metabolism, mitochondrial function, cell cycle control, and apoptosis, including upregulation of COX6C (Log2FC = 2.07) and downregulation of CDK4 (Log2FC = −1.26). These findings provide mechanistic insights and underscore the translational potential of postbiotics in lymphoma treatment. Further preclinical and clinical investigations are warranted to explore their role in therapeutic regimens.

Global interest in natural health products (NHPs) as complementary or alternative treatments is growing, especially among midlife women, due to their diverse health needs. Despite increased NHP use and benefits suggested by traditional use, the available scientific evidence supporting NHP efficacy and safety is often inconsistent, leading to hesitancy among health professionals about their use, even when reasonable evidence exists. Here, we offer a multidisciplinary perspective on optimizing NHP use alongside conventional clinical management in midlife women’s health. We advocate for robust systematic frameworks to generate and evaluate evidence from well-designed clinical studies, employing methodologies like those used for conventional medicines, but adapted to address the unique complexities of NHPs. We highlight key considerations for designing and developing NHP formulations: understanding differences in the activity spectrum of distinct extracts, the bioavailability of active compounds, and the chemical forms of the products. We also emphasize the importance of effectively communicating evidence on NHPs and its implications to health professionals and consumers, so as to maximize therapeutic benefits and minimize potential health risks. Essential actions include incorporating NHP education into continuing education programs for health professionals and enhancing public health literacy to promote safe, responsible, and informed use among consumers. Evidence-based approaches and multidisciplinary collaborations will help drive these essential actions and accelerate the complementary use of NHPs in improving health outcomes.

Lymphoma continues to pose a serious challenge to global health, underscoring the urgent need for new therapeutic strategies. Recently, the gut microbiome has been shown to play a potential role in regulating immune responses and influencing cancer progression. However, its molecular mechanisms of action in lymphoma remain poorly understood. This study investigates the antiproliferative and apoptotic activities of gut microbiota-derived metabolites, specifically nisin (N) and urolithin B (UB), individually and in combination 7:3 (5750 μM), against the human lymphoma cell line HKB-11. Comprehensive evaluations were performed using Alamar Blue viability assays, combination index (CI) analyses, reactive oxygen species (ROS) quantification, flow cytometry for apoptosis detection, and advanced bottom-up proteomics analyses. N and UB exhibited potent antiproliferative activity, with the 7:3 combination demonstrating strong synergistic effects (CI < 1), significantly enhancing apoptosis (p < 0.01) and ROS production (p < 0.0001) compared to the untreated control. Proteomics analyses revealed substantial alterations in proteins crucial to ribosomal biogenesis, mitochondrial function, cell cycle control, and apoptosis regulation, including a marked downregulation of ribosomal proteins (RPS27; Log2FC = −3.47) and UBE2N (Log2FC = −0.60). These findings highlight the potential of N and UB combinations as a novel and practical therapeutic approach for lymphoma treatment, warranting further in vivo exploration and clinical validation.

Lymphoma remains a significant global health burden, necessitating innovative, targeted therapeutic strategies. Nisin (N), a bacteriocin produced by Lactococcus lactis, has demonstrated antimicrobial and anticancer properties through membrane disruption and apoptotic induction. Urolithin B (UB), a gut microbiota-derived metabolite of ellagitannins, has shown anti-inflammatory and antiproliferative activities in various cancer models. Vincristine (Vinc), a common anti-lymphoma drug, disrupts microtubule formation, leading to cell cycle arrest and apoptosis in cancer cells. This study explored the antiproliferative and pro-apoptotic effects of a triple combination therapy comprising N, UB, and Vinc against human lymphoma cell lines (HKB-11 and Hs 313.T). This study systematically evaluated the synergistic efficacy of both monotherapy and dual and triple combinations and molecular mechanisms using Alamar Blue viability assays, combination index (CI) modelling, reactive oxygen species (ROS) quantification, annexin V/7-AAD flow cytometry, and bottom-up label-free proteomics. The potential cytotoxicity of the combination on normal stromal HS-5 cells was also assessed using the Alamar Blue assay. The N: UB: Vinc combination at 2240: 210: 0.94 µM demonstrated potent synergy (CI values 0.31–0.50 at IC90 - IC95) and induced near-complete growth inhibition (> 99%) in both lymphoma cell lines with reduced toxicity (42.09 ± 1.21% viability) toward normal stromal HS-5 cells. ROS analysis revealed significant oxidative stress, while flow cytometry confirmed enhanced apoptosis (p < 0.0001) in the combination groups. Proteomic profiling of the combination N: UB: Vinc at 2450.94 µM uncovered distinct molecular responses, including upregulation of MAP1LC3B2 (Log2FC = 1.4), GMNN (Log2FC = 1.3), and SLC38A2 (Log2FC = 1.5), promoting apoptosis, cell cycle regulation, and mTOR signaling inhibition. Concurrently, key oncogenic and metabolic proteins were downregulated, including NNMT (Log2FC = –2.9), PLTP (Log2FC = –2.5), and CYP4X1 (Log2FC = –2.0), which implicated the suppression of MAPK-Akt signaling, ferroptosis activation, and lipid metabolism disruption. These results established a mechanistic rationale for combining postbiotics such as N and UB with standard chemotherapy, highlighting a promising avenue for safer and more effective lymphoma management in the future.

Background: Inflammation and oxidative stress are key mechanisms in underlying skin conditions like psoriasis and eczema. While many plants, including Australian native plants, are proposed to target these pathways due to their phytochemical content, studies on whole extracts and their synergistic effects remain limited. Objectives: This study aimed to investigate individual and combined effects of whole plant extracts on skin protection and healing, focusing on their anti-inflammatory and antioxidant properties. Methods: The antioxidant potential of the individual and combined plant extracts were investigated on 2,2-diphenyl-1-picrylhydrazyl (DPPH) and reactive oxygen species (ROS) assay followed by luciferase assay in MCF-7 AREc32 cells for nuclear factor erythroid 2-related factor 2 (Nrf2) activation. The anti-inflammatory activities were investigated on lipopolysaccharide (LPS)-induced RAW 264.7 murine macrophages for the inhibition of nitric oxide (NO), tumour necrosis factor (TNF)-α, and interleukin (IL)-6. Synergistic interaction was determined by the combination index model (CI < 1). Combination(s) showing synergistic and optimal activity were further investigated on LPS-induced human dermal fibroblasts (HDF) cells for IL-6 inhibition and wound healing activity. Results: Three of the tested Australian native plant extracts demonstrated prominent antioxidant and anti-inflammatory activities including bitter orange, mountain pepper berry and native river mint. In particular, their three-way combination (1:1:1, w/w) showed prominent synergistic (CI < 1) in reducing NO and IL-6, along with enhanced Nrf2 activation. In LPS-inflamed HDF cells, the combination maintained synergistic inhibition of IL-6 levels and promoted wound healing response. Conclusions: These findings highlight the therapeutic potential of Australian native plant as a whole extract for skin protection and repair attributed to antioxidant and anti-inflammatory activities. The observed synergistic anti-inflammatory and antioxidant effects support their use in the development of new cosmetic formulations for skin.

Phytochemical investigation of the Australian rainforest plant Cryptocarya rhodosperma B. Hyland (Lauraceae) led to the isolation and structural elucidation of seven new unique spiroketals fused with an α,β-unsaturated δ-lactone, namely, rhodospermals A-G (1 - 7), and a new alkylbenzodioxole α,β-unsaturated-δ-lactone rhodopyrone A (8) along with the known compounds EBC-23 (9) and EBC-73 (10). The chemical structures of these compounds were established by NMR spectroscopic data analysis, relative stereochemistry confirmed by distinct J coupling, NOESY correlations, and a close comparison of the NMR data and optical rotation of the previously reported compounds (9, 10). X-ray crystallography analysis and Mosher ester analysis of 1 confirmed the absolute stereochemistry of the fused spiroketal with an α,β-unsaturated δ-lactone. A plausible identical stereochemistry of the common fused spiroketal with an α,β-unsaturated δ-lactone observed in the remaining analogues (2-7) was proposed. The absolute stereochemistry of 8 was determined by performing a Mosher ester analysis and distinct J coupling. Compounds 1-10 exhibited cytotoxic activity in several cancer cell lines, highlighting their potential use in the treatment of human tumors.

Chronic neuroinflammation plays a central role in the development and progression of numerous neurodegenerative disorders, including Alzheimer’s, Parkinson’s, and Huntington’s diseases. Non-invasive imaging approaches capable of tracking neuroinflammatory processes over time are essential for elucidating disease mechanisms and evaluating emerging therapies. Among these, positron emission tomography (PET) using translocator protein (TSPO) ligands has emerged as a powerful tool to visualize glial activation in vivo. In this study, we assessed the potential of the TSPO radioligand 18F-PBR111 for imaging neuroinflammation in the GFAP-IL6 transgenic mouse model, which chronically overexpresses interleukin-6 (IL-6) under the astrocyte-specific GFAP promoter. Dynamic PET/CT imaging was performed in GFAP-IL6 and age-matched C57BL/6 wild-type mice, followed by ex vivo validation using immunohistochemistry and autoradiography. We observed a two-fold increase in cerebellar 18F-PBR111 uptake in GFAP-IL6 mice, alongside elevated binding of the alternative TSPO ligand 125I-CLINDE. Immunostaining confirmed increased TSPO and Iba1 expression, with clear co-localization indicating activated microglia. These results demonstrate a strong correlation between the in vivo PET signal and underlying microglial activation. Our findings validate 18F-PBR111 as a reliable biomarker for chronic neuroinflammation in a model characterized by astrocyte-driven IL-6 overexpression. This work underscores the utility of TSPO-targeted PET imaging for longitudinal monitoring and therapeutic evaluation in neuroinflammatory conditions and supports its use in translational research targeting glial activation.

Curcumin is widely used for its antioxidant and anti-inflammatory properties, but its poor oral bioavailability has driven the development of advanced formulations such as CAVACURMIN®, a γ-cyclodextrin-based curcumin complex with enhanced absorption. Given recent regulatory scrutiny of high-bioavailability curcumin products, we evaluated the subacute oral safety of CAVACURMIN® in Wistar rats. Animals received 2000 mg/kg/day (low dose) or 3500 mg/kg/day (high dose) for 28 days, with controls receiving vehicle or γ-cyclodextrin alone. No mortality or systemic toxicity occurred, except for one incidental death unrelated to treatment. Transient post-dosing signs (salivation, bedding displacement) were attributed to local sensory or irritant effects. Clinical chemistry showed modest, non-adverse variations—including decreased urea (up to −25% in males) and increased albumin (up to +9% in females)—that were not associated with pathological or clinical abnormalities. All other parameters, including body weight, food intake, haematology, organ weights (except for a small, non-adverse liver-weight increase in high-dose females), and gross pathology, were comparable to controls. These findings demonstrate that CAVACURMIN® was well tolerated at doses up to 3500 mg/kg/day and provide a basis for subsequent OECD 408-compliant 90-day toxicity studies.

Subjective Cognitive Impairment (SCI) is a self-perceived worsening of cognitive decline, carrying an increased risk of developing Mild Cognitive Impairment (MCI) and Alzheimer's Disease (AD). Due to the self-report nature of SCI, an understanding of the biological mechanisms that contribute to an increased dementia risk is needed. This study aims to assess the differences in resting state electroencephalography (EEG) (eyes-open, eyes-closed; EO, EC) between older adults with SCI and healthy controls (HCs) utilising frequency principal components analysis (fPCA), a novel data driven approach. Participants (n = 14 per group: SCI, HCs) were matched on age, sex, years of education, mood, cognition, and pre-morbid function. Continuous resting EEG was recorded during 2-minute conditions (EO, EC) and were submitted to 4 separate fPCAs (each condition, group). Corresponding components were assessed between groups and conditions, correlated with demographics, mood, and cognition variables; multivariate logistic regression was also carried out. Component amplitudes were larger in HCs for delta-theta and alpha-beta, while theta-alpha was larger for SCI. DASS anxiety scores contributed to higher amplitudes for HCs in EO delta-theta and alpha-beta, while male sex and depressive symptoms contributed to higher amplitudes for the SCI group in EO and EC theta-alpha. Findings demonstrate a distinct divergent signature of neurological activity in older people with SCI, despite normal objective cognitive function. This is the first fPCA study to investigate neuronal differences between HCs and older adults with SCI at rest. Novel confounders and effect modifiers were identified that should be controlled in future studies.

Emerging research has revealed a complex bidirectional interaction between the gut microbiome and cannabis. Preclinical studies have demonstrated that the gut microbiota can significantly influence the pharmacological effects of cannabinoids. One notable finding is the ability of the gut microbiota to metabolise cannabinoids, including Δ9-tetrahydrocannabinol (THC). This metabolic transformation can alter the potency and duration of cannabinoid effects, potentially impacting their efficacy in cancer treatment. Additionally, the capacity of gut microbiota to activate cannabinoid receptors through the production of secondary bile acids underscores its role in directly influencing the pharmacological activity of cannabinoids. While the literature reveals promising avenues for leveraging the gut microbiome–cannabis axis in cancer therapy, several critical considerations must be accounted for. Firstly, the variability in gut microbiota composition among individuals presents a challenge in developing universal treatment strategies. The diversity in gut microbiota may lead to variations in cannabinoid metabolism and treatment responses, emphasising the need for personalised medicine approaches. The growing interest in understanding how the gut microbiome and cannabis may impact cancer has created a demand for up-to-date, comprehensive reviews to inform researchers and healthcare practitioners. This review provides a timely and invaluable resource by synthesizing the most recent research findings and spotlighting emerging trends. A thorough examination of the literature on the interplay between the gut microbiome and cannabis, specifically focusing on their potential implications for cancer, is presented in this review to devise innovative and effective therapeutic strategies for managing cancer.

Phytochemical investigation of the leaves of Polyscias australiana (F.Muell.) Philipson (family Araliaceae) led to the isolation and identification of two new analogues belonging to the rare dammarane-type triterpene glycosides, polysciasosides B (1) and C (2). Also isolated in high yields from this plant was the known saponin, β-hedrin (3). The two new polysciasoside analogues exhibited no anti-inflammatory activity (inhibitory effects on NO inhibition and cell viability in RAW 264.7 macrophages) or cytotoxic activity against AGS gastric adenocarcinoma or the MCF7 breast adenocarcinoma cell lines. In contrast, the known compound β-hedrin exhibited potent anti-inflammatory and cytotoxicity in these biological assays.

Despite extensive research, determining the optimal level of sunlight exposure for human health remains a challenge, emphasizing the need for ongoing scientific inquiry into this critical aspect of human well-being. This review aims to elucidate how different components of the solar spectrum, particularly near-infrared (NIR) radiation and ultraviolet radiation (UVR) affect human health in diverse ways depending on factors such as time of day and duration of exposure. Sunlight has beneficial effects from the production of melatonin by NIR and vitamin D by UVB. Sunlight also causes harmful effects as evidenced by oxidative stress and DNA damage. Exposure to morning and evening sunlight when the UV index is below 3 is suggested to be beneficial for harnessing its positive effects while avoiding the harmful effects of UVR when the UV index is 3 or higher. Understanding the optimal timing and duration of sunlight exposure is crucial for harnessing its beneficial effects while minimizing its harmful consequences by adopting appropriate sun protection measures. By adhering to sun protection guidelines when the UV index is 3 or more and incorporating strategic exposure to NIR rays when the UV index is less than 3, individuals can optimize their health outcomes while mitigating the risks associated with sun exposure. Given that the effects of sun exposure can be both harmful and beneficial, and Australia’s unique geographical position where it experiences the highest levels of exposure to sunlight, it is vital to understand the appropriate level and timing of sun exposure to live healthy under the Australian sun.

Our ongoing exploration of Australian rainforest plants for the biodiscovery of anti-inflammatory agents led to the isolation and structural elucidation of eight new arylalkenyl alpha,beta-unsaturated-delta-lactones, triplinones A-H (1-8), from the leaves of the Australian rainforest plant Cryptocarya triplinervis B. Hyland (Lauraceae). The chemical structures of these compounds were established by NMR spectroscopic data analysis, while their relative and absolute configurations were established using a combination of Mosher ester analysis utilizing both Riguera's and Kishi's methods, ECD experiments, and X-ray crystallography analysis. Compounds 1-8 exhibited good inhibitory activities toward nitric oxide (NO) production in lipopolysaccharide (LPS) and interferon (IFN)-gamma induced RAW 264.7 macrophages, in particular compounds 1-3 and 5, with IC50 values of 7.3 +/- 0.5, 6.0 +/- 0.3, 5.6 +/- 0.3, and 5.4 +/- 2.5 mu M, respectively.