Objective: To characterize the diversity and composition of bacterial communities in bat fecal samples under distinct ecological and biological conditions and to investigate the phylogenetic relationships of selected bacterial lineages with clinically relevant taxa. Methods: Publicly available 16S rRNA gene sequencing data from 194 fecal samples covering 20 bat species from South America, Europe, Asia, and Africa were reanalyzed using DADA2 and the SILVA database. Alpha and beta diversity, taxonomic composition, and community differences according to host diet, habitat, sex, and geographic region were evaluated. Phylogenetic analyses were performed on amplicon sequence variants assigned to Pseudomonas, Staphylococcus, Clostridium, and Streptococcus. Results: A total of 3 778 110 reads passed quality filtering, representing 123 bacterial families and 203 genera. Proteobacteria (57%) and Firmicutes (40%) predominated, with Pseudomonas, Staphylococcus, and Carnobacterium among the most abundant genera. Microbial composition and diversity varied significantly according to diet, habitat, sex, and geographic region. Frugivorous bats showed the highest alpha diversity, whereas piscivorous bats showed the lowest, and Rousettus aegyptiacus exhibited the greatest bacterial richness. Bats inhabiting forest and cave habitats possessed higher bacterial richness, while communities from freshwater and coastal aquatic habitats were less diverse. Males showed higher relative abundance of Staphylococcus, whereas females were enriched in Pseudomonas. Distinct taxonomic signatures were linked to dietary guilds. Insectivorous bats were enriched in Gammaproteobacteria, Pseudomonadales, and Moraxellaceae; frugivorous bats were enriched in Lactobacillales and Streptococcus; and piscivorous bats were enriched in Firmicutes, including Staphylococcaceae and Clostridium. Sixty-two genera containing species with recognized pathogenic potential were identified. Phylogenetic analyses revealed amplicon sequence variants affiliated with Pseudomonas, Clostridium, and Streptococcus clustering with or related to clinically relevant lineages, such as Clostridioides difficile and Streptococcus pneumoniae. Conclusions: Bat fecal bacterial communities are highly diverse and vary significantly under different ecological and biological conditions. Detection of bacterial genera containing clinically relevant species and the phylogenetic proximity of selected amplicon sequence variants to known pathogens support further genomic, functional, and epidemiological studies to clarify their pathogenic and zoonotic relevance.

Objective: To investigate whether ganoderic acid can alleviate streptozotocin-induced diabetic retinopathy and explore its underlying mechanisms. Methods: Streptozotocin (55 mg/kg) combined with nicotinamide (100 mg/kg body weight) was used to establish a diabetes mellitus rat model. Rats were then orally administered ganoderic acid at doses of 12.5, 25, and 50 mg/kg. Body weight, blood glucose, organ weights, and serum insulin levels were determined. Hepatic and renal biochemical indices, as well as markers related to oxidative stress, angiogenesis, inflammation, and apoptosis in retinal tissues, were also assessed. Results: Ganoderic acid treatment significantly (P<0.001) lowered blood glucose and improved insulin levels and body and organ weights. The treatment remarkably attenuated blood-retinal barrier disruption, reduced acellular capillaries, and ameliorated hepatic and renal pathological changes, accompanied by decreased levels of IL-1β, TNF-α, IL-6, IL-17, COX-2, and PGE₂. In addition, ganoderic acid upregulated Nrf2 and HO-1 and modulated the mRNA expression of Bax and Bcl-2. Conclusions: Ganoderic acid ameliorates streptozotocin-induced diabetic retinopathy by inhibiting inflammation and apoptosis and enhancing antioxidant activities.

Objective: To evaluate the neuroprotective effects of Rosa moschata leaf extract against sodium arsenate-induced cognitive impairment in rats.
Methods: Memory impairment was induced with oral sodium arsenate (10 mg/kg) in rats. Rosa moschata leaf extract was administered orally at 150, 300, and 600 mg/kg for three weeks. Behavioral tests, measurement of oxidative stress parameters and neurotransmitter levels, histopathological assessment, and real-time PCR were performed.
Results: Rosa moschata leaf extract dose-dependently increased antioxidant enzyme activities and reduced malondialdehyde levels in rats with sodium arsenate-induced cognitive impairment compared with untreated controls. It also inhibited acetylcholinesterase activity, and enhanced dopamine, serotonin, and noradrenaline levels. Rosa moschata leaf extract significantly improved behavioral parameters in open field test, Y-maze test, Morris water maze test, and elevated plus maze test in a dose-dependent manner. Quantitative PCR demonstrated reduced α-synuclein expression and downregulation of neuroinflammatory mediators after treatment.
Conclusions: Rosa moschata leaf extract exhibits marked neuroprotective effects against sodium arsenate-induced cognitive impairment. These findings support its potential as a promising therapeutic candidate for managing memory impairment and related neurodegenerative disorders.

Objective: To determine whether cristazine inhibits HPV-positive cervical cancer cells and to elucidate its underlying mechanisms.
Methods: HeLa cells were treated with varying concentrations of cristazine, and cell viability, intracellular ROS, apoptosis, and apoptosis-related gene and protein expression were assessed using WST-1, DCF-DA flow cytometry, Annexin V-FITC/PI staining, quantitative RT-PCR, and Western blotting. Additionally, CaSki and SiHa cells were evaluated in viability assays, with selected ROS and apoptosis measurements performed in CaSki cells.
Results: After 24 h of treatment, cristazine reduced HeLa cell viability with an IC₅₀ of 0.223 μM and increased intracellular ROS and apoptotic populations. Caspase inhibition substantially restored viability and reduced apoptosis. Cristazine also increased TP53, CDKN1A, BAX, BCL2, and CASP3 expression, and reduced HPV18 E6/E7 expression. Additionally, Western blotting showed upregulated p53, p21 and Bax/Bcl-2 ratio, and increased cleavage of caspases-3, -8, -9, and -12 and PARP after cristazine treatment. DAPI staining showed chromatin condensation, while wound healing assays demonstrated reduced wound closure following cristazine treatment.
Conclusions: Cristazine suppresses cervical cancer cell growth via coordinated ROS-associated, p53-driven, and caspase-dependent apoptotic signaling, highlighting its potential as a marine-derived anticancer candidate that warrants further investigation.