Bladder cancer is one of the causes of cancer‑related death and has a high mortality rate due to its metastatic ability. Naringenin, a bioactive compound predominantly found in citrus fruits, exhibits several cellular functions, including anti‑oxidant, ‑lipidemia and ‑cancer abilities. However, the effects of naringenin on bladder cancer cells are yet to be elucidated. The present study investigated the molecular mechanisms underlying the effects of naringenin on the migration of TSGH‑8301 bladder cancer cells. Treatment with naringenin at doses ranging between 0 and 300 µM over a period of 24 h was found to reduce cell viability. Furthermore, zymography and western blot analysis revealed that naringenin reduced the expression of matrix metalloproteinase (MMP)‑2 in a dose‑dependent manner, and repressed its activity. Naringenin also reduced TSGH‑8301 cell migration in a concentration‑dependent manner, as evidenced by wound healing and Transwell® assays. In addition, naringenin was found to inhibit AKT activity and block the nuclear translocation of nuclear factor κ‑light‑chain‑enhancer of activated B cells. In conclusion, the findings of the present study show that naringenin is capable of inhibiting bladder cancer cell migration through the downregulation of the AKT and MMP‑2 pathways.

Microsomal triglyceride transfer protein (MTTP) is an endoplasmic reticulum resident protein that is essential for the assembly and secretion of triglyceride (TG)-rich, apoB-containing lipoproteins. Although the function and structure of mammalian MTTP have been extensively studied, how exactly MTTP transfers lipids to lipid acceptors and whether there are other biomolecules involved in MTTP-mediated lipid transport remain elusive. Here we identify a role in this process for the poorly characterized protein PRAP1. We report that PRAP1 and MTTP are partially colocalized in the endoplasmic reticulum. We observe that PRAP1 directly binds to TG and facilitates MTTP-mediated lipid transfer. A single amino acid mutation at position 85 (E85V) impairs PRAP1's ability to form a ternary complex with TG and MTTP, as well as impairs its ability to facilitate MTTP-mediated apoB-containing lipoprotein assembly and secretion, suggesting that the ternary complex formation is required for PRAP1 to facilitate MTTP-mediated lipid transport. PRAP1 is detectable in chylomicron/VLDL-rich plasma fractions, suggesting that MTTP recognizes PRAP1-bound TG as a cargo and transfers TG along with PRAP1 to lipid acceptors. Both PRAP1-deficient and E85V knock-in mutant mice fed a chow diet manifested an increase in the length of their small intestines, likely to compensate for challenges in absorbing lipid. Interestingly, both genetically modified mice gained significantly less body weight and fat mass when on high-fat diets compared with littermate controls and were prevented from hepatosteatosis. Together, this study provides evidence that PRAP1 plays an important role in MTTP-mediated lipid transport and lipid absorption.

The capability of Chhit-Chan-Than extract powder (CCTEP, 10% aqueous Ocimum gratissimum L. extract) to protect against carbon tetrachloride (CCl4)-induced oxidative stress and hepatotoxicity in vivo was investigated. Wistar rats were divided into five groups. Group A was a normal control group given only vehicle; Group B, the hepatotoxic group, was injected intraperitoneally twice a week with repeated 8% CCl4/olive oil (0.1 mL/100 g of body weight); Groups C–E, extract-treated groups received CCl4 and different doses of CCTEP (100 mg/kg and 200 mg/kg) or silymarin (200 mg/kg of body weight) daily by gavage for 8 weeks, respectively. The results showed that the CCl4-induced histopathogical changes may be prevented by CCTEP through reducing the intercellular collogen stack, dropping blood serum alanine aminotransferase and aspartate aminotransferase levels, and restoring the catalase activity and glutathione content. The hepatoprotective properties were further confirmed by the marked improvement in histopathological examination and by quantitative steatosis-fibrosis scoring. The above results suggest that CCTEP is able to prevent the liver inflammation and fibrosis induced by repeated CCl4 administration, and the hepatoprotective effects might be correlated partly with its antioxidant and free radical scavenging effects

Increased cell death of cardiomyocyte by oxidative stress is known to cause dysfunction of the heart. O. gratissimum is one of the more well‐known medicinal plants among the Ocimum species and widely used in treatment of inflammatory diseases. In this study, we hypothesized that aqueous extract of O. gratissimum leaf (OGE) may protect myocardiac cell H9c2 from oxidative injury by hydrogen peroxide (H₂O₂). Our results revealed that OGE pretreatment dose‐dependently protects H9c2 cells from cell death when exposed to H₂O₂. Additionally, DNA condensation induced by H₂O₂ was also reduced by OGE pretreatment, suggesting that Ocimum gratissimum extract may attenuate H₂O₂‐induced chromosome damage. Further investigation showed that OGE pretreatment inhibited H₂O₂‐induced activation of caspase‐3 and caspase‐9, as well as H₂O₂‐induced upregulation of proapoptotic Apaf‐1 and the release of cytosolic cytochrome c, but has little effect on the activation of caspase‐8. Additionally, OGE pretreatment significantly upregulated Bcl‐2 expression and Akt phosphorylation, and slightly affected the phosphorylation of mitogen‐activated protein kinases including p38 MAPK and JNK. Taken together, our findings revealed that Ocimum gratissimum extract effectively inhibited the mitochondrial pathway and upregulated Bcl‐2 expression, which may be important in protecting H9c2 cells from H₂O₂‐induced cell death.

The present study evaluated the effects of physiological serum estrogen during the menstrual cycle on glutathione (GSH) and catalase activities. The sample included 43 healthy females between the ages of 22 and 51 years. The subjects were divided into two groups according to the stage of the menstrual cycle. Group A consisted of 16 samples extracted between days 10 and 20 from the first day of menstruation when estrogen levels were considered to be at their highest. Group B consisted of 27 samples extracted during other times of the estimated 30 days of menstruation. Data showed that the estrogen level in group A (184±106 pg/ml) was higher than that in group B (105±56 pg/ml) (P<0.01). The GSH and catalase levels in group A (4.4±2.3 µg/mg and 210±72 IU/mg, respectively) were also significantly higher compared to the levels in group B (3.2±1.8 µg/mg and 168±62 IU/mg, respectively) (P <0.05). Spearman's rank correlation showed that the expression of catalase in red blood cells significantly correlated with serum estrogen level but not with GSH. However, the changes in estrogen plasma levels, erythrocyte GSH level and catalase activity suggested that the consumption of GSH and catalase in erythrocyte during the menstrual cycle may be associated with the level of estrogen present in the bloodstream.

Treatment of advanced hepatocellular carcinoma (HCC) has exhibited a poor overall survival rate of only six to ten months, and the urgency of the development of more effective novel agents is ever present. In this line of research, we aimed to investigate the effects and inhibitive mechanisms of aqueous Ocimum gratissimum leaf extract (OGE), the extract of Ocimum gratissimum, which is commonly used as a therapeutic herb for its numerous pharmacological properties, on malignant HCC cells. Our results showed that OGE decreased the cell viability of HCC SK-Hep1 and HA22T cells in a dose-dependent manner (from 400 to 800 µg/mL), while there is little effect on Chang liver cells. Moreover, cell-cycle analysis shows increased Sub-G1 cell count in SK-Hep1 and HA22T cells which is not observed in Chang liver cells. These findings raise suspicion that the OGE-induced cell death may be mediated through proteins that regulate cell cycle and apoptosis in SK-Hep1 and HA22T cells, and further experimentation revealed that OGE treatment resulted in a dose-dependent decrease in caspase 3 and PARP expressions and in CDK4and p-ERK1/2expressions. Moreover, animal tests also exhibited decreased HCC tumor growth by OGE treatment. We therefore suggest that the inhibition of cell viability and tumor growth induced by OGE may be correlated to the alteration of apoptosis-related proteins.