Riceberry has recently been acknowledged for its beneficial pharmacological effects. Riceberry bran oil (RBBO) exhibited anti-proliferation activity in various cancer cell lines. However, animal studies of RBBO on anti-carcinogenicity and its molecular inhibitory mechanism have been limited. This study purposed to investigate the chemopreventive effects of RBBO on the carcinogen-induced liver and colorectal carcinogenesis in rats. Rats were injected with diethylnitrosamine (DEN) and 1,2-dimethylhydrazine (DMH) and further orally administered with RBBO equivalent to 100 mg/kg body weight of γ-oryzanol 5 days/week for 10 weeks. RBBO administration suppressed preneoplastic lesions including hepatic glutathione S-transferase placental form positive foci and colorectal aberrant crypt foci. Accordingly, RBBO induced hepatocellular and colorectal cell apoptosis and reduced pro-inflammatory cytokine expression. Interestingly, RBBO effectively promoted the alteration of gut microbiota in DEN- and DMH-induced rats, as has been shown in the elevated Firmicutes/Bacteroidetes ratio. This outcome was consistent with an increase in butyrate in the feces of carcinogen-induced rats. The increase in butyrate reflects the chemopreventive properties of RBBO through the mechanisms of its anti-inflammatory properties and cell apoptosis induction in preneoplastic cells. This would indicate that RBBO containing γ-oryzanol, phytosterols, and tocols holds significant potential in the prevention of cancer.

Purple rice has gained attention for its health promoting potential due to a high content of bioactive phytochemicals. The heat generated during cooking alters the quality and quantity of nutrients and phytochemicals in food. This study aimed to investigate the phytochemical profile and chemopreventive properties of cooked glutinous purple rice using cell-based assays and a rat model. Purple rice was cooked in a rice cooker and was then further extracted with solvents to obtain dichloromethane and methanol extracts. The methanol extracts of glutinous purple rice contained great amounts of phenolics, flavonoids, and anthocyanins. Protocatechuic acid (2.26–5.40 mg/g extract) and cyanidin 3-glucoside (34.3–65.7 mg/g extract) were the major phenolic acid and anthocyanin contents, respectively. After cooking, the content of anthocyanins, γ-oryzanols, and phytosterols decreased, while the amount of some phenolic acid and tocol contents increased. Methanol extracts of glutinous purple rice inhibited reactive oxygen species production about 60% in PMA-treated peripheral blood mononuclear cells, reduced nitric oxide formation in LPS-induced RAW 264.7 cells (26–39% inhibition), and exhibited antimutagenicity against several mutagens using the Ames test, but dichloromethane extracts presented only mild anti-inflammatory activities. Although methanol extracts induced mild mutagenicity (mutagenic index 2.0–2.5), they did not induce micronucleated hepatocyte formation and certain hepatic CYP450 isozyme activities in rats. However, the mutagenicity of the methanol extract significantly declined after cooking. In summary, the methanol extract of the cooked glutinous purple rice might be a promising cancer chemopreventive fraction, which was neither genotoxic nor posing adverse effects on phytochemical–drug interaction in rats.

Hepatocarcinogenesis is linked to environmental factors, with microplastics (MPs) emerging as a global environmental concern that may contribute to liver injury. However, the impact of MPs on the early stages of hepatocarcinogenesis has been largely ignored. Here we investigated the impact of long-term MP exposure on the formation of preneoplastic lesions during hepatocarcinogenesis induced by diethylnitrosamine (DEN) in rats. Rats were injected with DEN to induce preneoplastic lesions, and then they were orally administered with 1 µm MPs 0.5 mg/kg body weight per day for 20 weeks. The results revealed that long-term exposure to MPs did not induce the formation of glutathione S-transferase placental form (GST-P)-positive foci as preneoplastic lesions during hepatocarcinogenesis in these animals, thereby indicating non-carcinogenicity. However, MP exposure resulted in a 1-fold increase in both the number and size of GST-P-positive foci in rats initiated with DEN compared to those treated with DEN alone. Accordingly, MP exposure led to a 0.61-fold increase in the index of proliferating cell nuclear antigen (PCNA)-positive cells in DEN-initiated rats when compared to DEN treatment alone. In addition, the composition of the gut microbiota was significantly altered, accompanied by various levels of short-chain fatty acids. Our results suggest that long-term MP exposure can promote pre-neoplastic lesion formation in DEN-induced rats by increased cell proliferation as well as alterations in the gut microbiota and short-chain fatty acid levels. This highlights the potential health risks associated with hepatocarcinogenesis linked to long-term exposure to MPs.

With the widespread use of antiretroviral therapy, human immunodeficiency virus (HIV) infection is considered to be a manageable chronic disease, but it is accompanied by an increased burden of comorbidities. Baise is an area characterized by a high incidence of HIV infection in Guangxi, China. However, research on its comorbidity patterns is limited. This study aims to clarify the burden, patterns, network features, and temporal evolution of comorbidities among HIV inpatients in Baise. We collected electronic medical records from 3,294 HIV patients hospitalized at Baise People’s Hospital between January 2019 and August 2024. The Apriori algorithm was employed to extract association rules between diseases, while Gephi was utilized to construct comorbidity social network diagrams of the data. The findings revealed that 99.48% of patients presented with two or more comorbidities, with a median of 9 comorbidities per patient. Notably, the median number of comorbidities peaked at 11–12 during 2021–2022, subsequently decreasing to 7 in 2023–2024. The comorbidity patterns transitioned from (B20 + B37 → B99) in 2019 to (E46 + B20 → E87 + D64) in 2021 and ultimately evolved into (J18 + E87 → E46) by 2023. Social network analysis indicated that electrolyte imbalances (E87), HIV-related infections (B20) and candidiasis (B37) served as the core disease nodes within the network, displaying close connections with numerous other disease nodes. The identified specific comorbidity patterns can serve as early warnings and screening tools in clinical practice and they underscore the necessity for multidisciplinary care for HIV patients.

Small heat shock proteins (sHSPs) are involved in a wide range of abiotic stresses, yet the functional roles of sHSP family genes in rubber tree salt tolerance remain largely uncharacterized. In this study, HbsHSP23.8a, a novel sHSP gene from rubber tree, was cloned and analyzed in detail. HbsHSP23.8a consists of a targeting peptide, an N-terminal domain, an α-crystallin domain (ACD), and C-terminal extensions. Additionally, putative dimer interface and conserved amino acid sequences were identified in the ACD and N-terminal domain of HbsHSP23.8a, respectively. HbsHSP23.8a transcripts were detected in different tissues and developmental stages of leaves, indicating that HbsHSP23.8a was associated with rubber tree growth and development. Besides tapping panel dryness (TPD), HbsHSP23.8a was also involved in low-temperature, high-salt, methyl jasmonate (MeJA), and ethephon (ET) responses. Under salt stress, overexpression of HbsHSP23.8a in transgenic tobacco plants exhibited greater plant height and fresh weight than wild-type (WT) plants. In addition, tobacco plants overexpressing HbsHSP23.8a increased the activities of antioxidant enzymes and decreased hydrogen peroxide (H₂O₂) accumulation and chlorophyll degradation under salt stress compared with the WT plants. Collectively, our results suggest that HbsHSP23.8a is related to rubber tree growth, TPD, leaf development, stress and hormone responses. Furthermore, heterologous expression of HbsHSP23.8a is associated with enhanced salt tolerance in transgenic tobacco, which may be attributed to elevated antioxidant enzyme activities, reduced cellular H₂O₂ accumulation, and alleviated chlorophyll degradation.