The administration of bovine hydroxyapatite-alendronate implant accelerates bone defect healing in an osteoporotic rat.

BACKGROUND: Bone fracture is the main consequence of osteoporosis, which may become a neglected disease. OBJECTIVE: This study aims to fabricate bovine hydroxyapatite-gelatine (BHA-GEL) based bone-implant with alendronate (ALE) in vivo. METHODS: Wistar rats were used for an osteoporotic animal model induced by ovariectomy. There were three groups: negative control, BHA-GEL implant, and BHA-GEL-ALE implant. Each group performed a defect by drilling the femur (diameter of 2.2 mm and depth of 2 mm). Observations on the closure of bone defects were performed by X-ray radiography at the second and sixth week after surgery. The mechanism of bone healing was observed by using hematoxylin-eosin (HE) staining and immunohistochemical technique with anti-vascular endothelial growth factor (VEGF) and anti-alkaline phosphatase (ALP) antibodies. RESULTS: The radiograph examination showed the implanted group had accelerated bone growth. In addition, the osteoblast, osteoclast and osteocyte had accelerated migration to the defect area. Moreover, the immunoreactive score (IRS) of VEGF at the sixth week in the BHA-GEL-ALE group was lower than the other groups. Meanwhile, the IRS of ALP in BHA-GEL-ALE was higher compared to other groups. CONCLUSION: The BHA-GEL-ALE implant accelerates the healing of bone defect in the osteoporotic rat by increasing the ALP expression and the total number of cells.

Attenuation of hyperplasia in lung parenchymal and colonic epithelial cells in DMBA-induced cancer by administering Andrographis paniculata Nees extract using animal model.

OBJECTIVES: This study was designed to evaluate the potential of Andrographis paniculata ethanolic extract to inhibit the increase in proliferation and induction of abnormal cell death. METHODS: The hyperplasia stage as an early stage of cancer development was induced by oral administration of 20 mg/Kg BW DMBA to SD rats twice a week for 5 weeks. There were five groups in this study include negative control, positive control, and treatment groups of DMBA induction followed by administration of A. paniculata ethanolic extract in doses equivalent to 10, 30 or 100 mg/Kg BW andrographolide once per day for 6 consecutive weeks. On the last day, rats were sacrificed, lung and colon tissues were collected. Histological examination by HE staining and immunohistochemistry using p53, telomerase, and caspase-3 antibodies were aimed at observing hyperplasia state in these tissues. RESULTS: DMBA induction to SD rats was able to produce hyperplasia in lung parenchymal and colon epithelial tissue. This can be showed by the increasing number of proliferated cells and as indicated by the number of brown-colored nuclei with sharper intensity. As well telomerase appears to be overexpressed strongly, while p53 and caspase-3 show low intensity. The administration of A. paniculata extract for 6 weeks showed a decrease in the number of cells that actively proliferate, a decrease in telomerase activity, and an increase in caspase-3 levels which indicate cellular death activity. CONCLUSIONS: A. paniculata ethanolic extract can inhibit the development of cancer at the hyperplasia stage by reducing telomerase activity and increasing apoptosis, marked by an increase of caspase-3 expressions.

The effect of various high-fat diet on liver histology in the development of NAFLD models in mice.

OBJECTIVES: Nonalcoholic fatty liver disease (NAFLD) is exceptionally common around the world. The development of NAFLD is increasing rapidly in the world, along with changes in lifestyle. Excess lipid intake is one of the risk factors for NAFLD. The NAFLD model is induced by a high-fat diet contains SFA, MUFA, and ῳ-6 PUFA. This study aims to assess the effect of high-fat diet variation on liver histology in developing NAFLD models in mice. METHODS: Thirty-six male mice (Balb/c) were divided into six groups fed a high-fat diet containing beef tallow 60%, beef tallow 45%, vegetable ghee, animal ghee + corn oil, vegetable ghee + corn oil for 28 days and compared to a control group fed a chow diet. All of the mice were fed with a high-fat diet in the form of pellets ad libitum for 28 days. Bodyweight and food intake were measured every day. At the last day of treatment, animals were sacrificed and the Liver were taken for histological analysis. RESULTS: This study showed that NAFLD model development was achieved in all group mice fed a high-fat diet with different degrees of NAFLD. Beef tallow 60% had the worst liver histology. CONCLUSIONS: Thus, based on this study, we found that high-fat diet variations influenced the development of NAFLD models in mice, particularly concerning liver histology.

Selective serotonin reuptake inhibitor fluvoxamine ameliorates stress- and NSAID-induced peptic ulcer possibly by involving Hsp70.

Background Selective serotonin reuptake inhibitors (SSRIs) have recently become potential candidates for a new therapeutic approach to ulcer and gastric bleeding. Heat shock protein 70 (Hsp70) plays an important role in cellular resistance to nonsteroidal anti-inflammatory drugs (NSAIDs). However, there is lack of evidence that fluvoxamine recruits Hsp70 to affect stress-induced gastric ulcer. Therefore, we investigated the effect of fluvoxamine on NSAID- and stress-induced gastric ulcer and the possible involvement of Hsp70. Methods ICR mice were used in the study. Stress induction was made by the water-immersion-plus-restraint method. NSAID-induced gastric ulcer was produced by oral administration of indomethacin. Fluvoxamine was given orally 30 min before stress induction and indomethacin treatment. Results Stress and indomethacin treatment significantly increased the ulcer index and intraluminal bleeding score. Stress and indomethacin treatment also significantly increased the expression of Hsp70. Fluvoxamine significantly decreased the ulcer index and intraluminal bleeding in both ulcer models. Moreover, fluvoxamine further increased the expression of Hsp70 in the gastric tissue of stress- and indomethacin-treated mice. Conclusions Our results indicate that fluvoxamine may have a protective effect against stress- as well as NSAID-induced gastric ulcer. In addition, the present study suggests the possible involvement of Hsp70 in the amelioration of gastric ulcer by fluvoxamine.