We report the simple one-step hydrothermal green synthesis of carbon dots (CDs) without any chemical reagents using mangosteen pulp (CDs1), peel (CDs2), and leaf (CDs3) extract as a green carbon source. In the aqueous medium, these CDs had a size of 8–15 nm with an energy gap of about 4 eV. The CDs emitted a bright green color under ultraviolet (UV) irritation with an average fluorescence quantum yield of the CDs of 1.6%. Moreover, the CDs contained various functional groups, such as C = C, C–C, C–O–C, C–O, C = O, C–H, and O–H, which were beneficial for enhancing their fluorescence property. Furthermore, the CDs were applied in the stain fluorescent imaging of myosatellite chicken stem cells and Vero cells. The CDs2 and CDs3 induced a strong fluorescence emission intensity of the strain cells, whereas CDs1 acted as the highest potential enhancer in cell proliferation as confirmed by its cellular viability which was the around four times that of the control. Therefore, the CDs were highly biocompatible and acted as enhancers in cell proliferation in myosatellite chicken stem cells and Vero cells. Thus, simple, cost-effective, scalable, and green synthetic approach-based CDs show promise for the development of selective organelle labeling and optical sensing probes.

The purpose of this study was to examine the characteristics of acetaminophen (APAP)-induced liver damage, using fluorescence bioimaging, serum biochemistry, and histopathology. At six weeks of age, eighteen mice were divided into three groups as group 1 (G1) as control, group 2 (G2) as fluorescence probe control and group 3 (G3) as APAP-treated. G3 mice were orally treated with APAP (800 mg/kg b.w.), while G1 and G2 mice were treated with 0.9% saline. Twenty-two hours after APAP treatment, G2 and G3 mice were intravenously treated with Annexin-Vivo 750 as probe, while G1 mice were treated with saline. Fluorescence bioimaging was performed at two hours after probe treatment. The mice were sacrificed and serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and lactate dehydrogenase were analyzed. Liver damage was examined by hematoxylin and eosin (H&E) staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. In vivo bioimaging, fluorescence intensity of the region of interest (ROI) was significantly increased in the livers of G2 and G3 mice compared with those in G1 mice (p<0.05 and p<0.01). In addition, ex vivo bioimaging confirmed that the fluorescence intensity of the ROI was significantly increased in the livers of G2 and G3 mice compared with those in G1 mice (p<0.05 and p<0.01). All examined serum parameters of G3 were significantly increased compared with G1 and G2 (p<0.05 and p<0.01). H&E examination showed acute hepatic cell necrosis in the livers of G3 mice, while there was no cell death in the livers of G1 and G2 mice. TUNEL staining also showed many cell death features in G3 mice, whereas no pathological findings were shown in G1 or G2 mice. In summary, fluorescence bioimaging showed the possibility of cell death detection in the livers of mice treated with APAP, and this was corroborated by serum chemistry and histopathological examination.

The purpose of this study was to investigate the lesions of a mouse collagen antibody-induced arthritis (CAIA) model using fluorescence bioimaging and micro-computed tomography (micro-CT) and to compare it with histopathological examination. Twelve mice were randomly divided into three groups: group 1 (G1) as control, group 2 (G2) as fluorescence probe control and group 3 (G3) as collagen antibodyinduced arthritis. The mice of G3 intravenously received anti-type II collagen 5-clone antibody cocktail (2 mg/mouse) on day 0 and intraperitoneally received lipopolysaccharide (50 μg/mouse) on day 3. On the while, the mice of G1 and G2 received 0.9% saline in equal volumes at equivalent times. Fluorescence bioimaging and micro-CT analysis were carried out to assess arthritis. Treatment with the collagen antibody cocktail increased the paw thickness of mice compared to those in both the control and probe-treated groups. Fluorescence bioimaging using a near infrared imaging agent showed high intensity in the joints of collagen antibody- treated mice, whereas those of control mice showed no signal. Micro-CT analysis of the knee joints of collagen antibody-treated mice showed rough and irregular articular appearance, whereas those of control mice showed normal appearance. Histopathological examination of the knee joints of collagen antibody-treated mice revealed destruction of cartilage and bony structure, synovial hyperplasia and infiltration of inflammatory cells. No cartilage destruction or inflammation was observed in control or probe control mice. Taken together, it is concluded that analyses of fluorescent bioimaging made it possible to evaluate CAIA lesions, comparable with those by micro-CT and histopathological examination in mice.