Angiogenesis, defined as the formation of new microvasculature from preexisting blood vessels and mature endothelial cells, plays a major role in wound healing and scar formation, and it is associated with inflammatory responses. Angiogenesis can occur in physiological conditions, such as during liver regeneration, and in pathological situations, such as during the progression of fibrosis to cirrhosis and also during tumor angiogenesis. Cellular cross-talk among liver sinusoidal endothelial cells (LSECs), hepatic stellate cells and hepatocytes is believed to play an important role in the angiogenesis process during both liver regeneration and development of cirrhosis. In addition to mature endothelial cells, bone marrow (BM)-derived circulating endothelial progenitor cells (EPCs) have been recently identified for their contribution to post-natal vasculogenesis/angiogenesis. In vivo, EPCs are mobilized into the peripheral blood in response to tissue ischemia or traumatic injury, migrate to the sites of injured endothelium and differentiate into mature endothelial cells. In our recent studies, we have explored the role of EPC-mediated angiogenesis in liver regeneration and/or cirrhosis. Results have demonstrated significantly increased endogenous levels of circulating EPCs in cirrhotic patients in comparison to the controls. Also, EPCs from cirrhotic patients have been observed to stimulate substantial angiogenesis by resident LSECs in vitro via paracrine factors such as vascular endothelial growth factor and platelet-derived growth factor. This review gives an overview of the angiogenesis process in liver regeneration and disease and discusses a new mechanism for intrahepatic angiogenesis mediated by BM-derived EPCs.
Background: Atherosclerosis is a chronic inflammation disease that is caused by the interaction between monocyte and endothelial injury in tunica intima. One of the major factor of atherosclerosis is dyslipidemia. Chronic dyslipidemia, especially hypercholesterolemia, can directly alter endothelial cell through reactive oxygen species (ROS) production that oxidizes low-density lipoprotein (LDL) to become oxidized LDL (Ox-LDL). Proinflammatory cytokines, the products of perivascular adipocyte tissue (PVAT), may draw macrophage. Macrophage then engulfs Ox-LDL and becomes foam cell within tunica intima. Lipoprotein-associated phospholipase A 2 (Lp-pLA 2) is an enzyme that cleaves Ox-LDL to become proatherosclerotic products. Darapladib, an Lp-pLA 2 inhibitor, is expected to inhibit atherosclerotic lesion progressivity. Aims and Objective: To know the effects of darapladib on Ox-LDL level, PVAT thickness, and foam cell number. Materials and Methods: This study used in vivo posttest controlled group design with two time series. Thirty male Sprague-Dawley rats divided into two group based on time series (8 weeks and 16 weeks). Each time serial was divided into three groups which were: standard diet group ;high-fat diet group; and dyslipidemia model with darapladib administration group with dose of 200 mg/200 g body weight (BW). The parameters that was measured in this study were lipid profile [total cholesterol, LDL/very-low-density lipoprotein (VLDL), and high-density lipoprotein (HDL)], Ox-LDL level, number of foam cells, and PVAT thickness. Result: Ox-LDL level and foam cell number decreased significantly (p = 0.000 and p = 0.005, respectively), while PVAT thickness did not show significant difference (p = 0.912). Conclusion: In this, study, it has been proven that darapladib decreases Ox-LDL levels and foam cell numbers but not in PVAT thickness, even though a decreasing pattern was observed histologically. Further study needed to know the optimum dosage of darapladib administration.
Curcumin has been shown to regulate the expression of genes implicated in tumor cell proliferation, metastasis, chemotherapy resistance, and angiogenesis. Endothelial progenitor cells (EPCs) have been recently described in the peripheral blood as cells contributing to both physiological and pathological angiogenesis. In the current study, we evaluated the effect of curcumin on these angiogenic cells. EPCs were isolated, expanded, and characterized ex vivo. These cells were then treated with different concentrations of curcumin. The formation of EPC colonies in culture and their proliferation was analyzed by 5'-bromo-2'-deoxyuridine assays in absence and presence of curcumin. Further, the expression of two important cell cycle inhibitory proteins, p21 and p53, in the curcumin- and culture medium-treated cells without curcumin was evaluated by intracellular flow cytometry. The results showed that there was a significant decrease in the formation of EPC colonies in culture. EPC proliferation was significantly inhibited by curcumin in a dose-dependent manner. Flow cytometry analysis showed a twofold increase in the expression of both p21 and p53 in curcumin-treated cells as compared to the medium-treated cells, suggesting that curcumin inhibits EPC growth by mainly inhibiting the G1 to S phase transition in the cell cycle. It would be further worthwhile to study the effect of curcumin on EPC-mediated angiogenic activity.
Metabolic inflammation (low-grade inflammation) remains an etiopathogenic key factor in the development of metabolic syndrome. Nuclear Factor Kappa Beta (NF-κβ) is a transcription regulator of genes having a role in immunity, the inflammatory response which can be associated with obesity-related pathological conditions like nonalcoholic fatty liver (NAFLD). Various stimuli, such as metabolic stress (hyperglycemia, ROS, fat metabolism) and proinflammatory cytokines (TNF-α, IL-6, IL-1β) could activate NF-κβ. This study was aimed to investigate the underlying molecular mechanisms of NAFLD in rats fed a modified AIN-93M HFHF (High Fat High Fructose) diet. The design of this study was experimental post-test only controlled group design. Thirty male Sprague Dawley rats were distributed into 2 treatment groups by a completely randomized design (CRD) technique. The sacrifice was performed after 17 weeks of treatment. NF-κβ expression was assessed by an immunohistochemical method (IRS score). The results showed there were significant differences in feed intake and energy intake between groups P1 and P2 (p = 0,000, p = 0,000). The average NF-κβ expression in the P2 group was significantly higher (p = 0.000) compared to the control group (P1). The correlation test between dietary intake and NF-κβ expression proved that there was a positive correlation between energy, carbohydrate and fat intake on NF-κβ expression (p = 0.001, 0.000, 0.046). However, there was a negative relationship between protein intake and NF-κβ expression (p = 0.000). This study concluded the modified AIN-93M HFHF diet increased NF-κβ expression in the liver tissue of male Sprague Dawley rats.
Lead is one of the pollutants widely spread in the environment because it is not easily decomposed. Lead can affect system functions such as the ovary and endometrium. Lead can trigger oxidative stress by reducing antioxidant enzymes and increasing Reactive Oxygen Species (ROS). Lead can also reduce Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH) levels by disturbing the hypothalamus. Chitosan is an antioxidant compound that can reduce the toxic effects of lead. The purpose of this study was to study the effects of chitosan administration on the diameter of antral follicles, the number of endometrial arterioles, and the thickness of endometrial rats after lead acetate exposure. This study was an experimental laboratory using a posttest-only control group design approach applied on 25 female rats aged 8 weeks old, body weight 125-175 grams. Lead and chitosan were given orally with a sonde. There were 5 groups, namely, negative control group (without any treatment), positive control group (lead 175mg/kg/BW), treatment group 1 (lead 175mg/kg/BW + chitosan 16mg/kg/BW, treatment group 2 (lead 175mg/kg/BW + chitosan 32mg/kg/BW), and treatment group 3 (lead 175mg/kg/BW + chitosan 64mg/kg/BW) for 30 days. The rats were sacrificed at proestrus phase, which was proven from vaginal swab. Observations were carried out using the Hematoxylin Eosin (HE) staining method. The observations were analyzed using One Way ANOVA and followed by Least Significant Differences (LSD) test. The results showed significant results (p-value <0.05). Chitosan can increase the diameter of the antral follicle, increase the number of endometrial arterioles, and increase the thickness of endometrial rats exposed by lead acetate.
Background: Nasopharyngeal carcinoma (NPC) is an endemic malignancy in Asia and in Indonesia with a high incidence and mortality. The high mortality rate of patients with NPC is caused by recurrence and metastases early in the disease process, even though they have been given a combination of standard NPC therapy, namely radiotherapy and chemotherapy. Recurrences generally occur after the initial modalities of radiotherapy. Toxicity due to therapy given over a long time can also increase mortality. This study aims to determine the expression of BCL11B in undifferentiated NPC and its correlation with LMP-1 so that it can provide an overview of the nature of CSC in NPC, which is thought to cause recurrence and metastases and provide a poor prognosis in patients with NPC. Methods: This study was an analytical observational study using a cross-sectional approach using 30 samples from nasopharyngeal biopsy tissue diagnosed with undifferentiated NPC at the anatomical pathology installation of Dr. Saiful Anwar General Hospital, Malang, Indonesia, between 2018-2020. LMP-1 and BCL11B expression was examined using the immunohistochemical method. Data analysis was performed univariate and bivariate with the help of SPSS software. Results: Statistical analysis using the Spearman correlation test between LMP-1 and BCL11B expression in undifferentiated NPC biopsy tissue showed a significant correlation (p=0.004) with a correlation coefficient of r=-0.511. Conclusion: The higher the expression of LMP-1, the lower the expression of BCL11B in nasopharyngeal biopsies of patients with undifferentiated.
Biji Pepaya (Carica papaya L.) merupakan salah satu bagian tanaman pepaya yang digunakan sebagai obat tradisional. Bahan aktif yang terdapat pada biji pepaya ini dapat mempengaruhi hormon yang dibutuhkan dalam perkembangan folikel ovarium sehingga berpengaruh pada berat ovarium. Penelitian ini bertujuan untuk mengetahui pengaruh pemberian ekstrak etanol biji terhadap jumlah folikel dan berat ovarium tikus putih betina galur wistar. Studi eksperimental menggunakan randomised post test only control group design dilakukan terhadap hewan coba tikus putih betina (Rattus norvegicus) galur Wistar. Pembagian kelompok meliputi kontrol (K) (0 mg/g BB), perlakuan 1 (P1) (0,1 mg/g BB), perlakuan 2 (P2) (0,2 mg/g BB), dan perlakuan 3 (P3) (0,3 mg/g BB). Parameter dalam penelitian ini meliputi jumlah folikel (folikel preantral dan antral) dan berat ovarium. Hasil penelitian menunjukkan bahwa kenaikan jumlah dosis ekstrak etanol biji pepaya yang diberikan tidak berbeda secara signifikan pada penurunan jumlah folikel preantral (p-value=0,974), namun berpengaruh secara signifikan pada penurunan jumlah folikel antral (p-value=0,044). Terbukti adanya perbedaan rerata berat ovarium yang signifikan pada kenaikan dosis ekstrak etanol biji pepaya yang diberikan kepada tikus putih betina (p-value=0,003). Hasil uji korelasi Rank Spearman yang bermakna hanya ditunjukkan dari hubungan dosis perlakuan dan jumlah folikel antral (p-value=0,016). Kesimpulan: pemberian ekstrak etanol biji pepaya terbukti dapat mempengaruhi penurunan jumlah folikel antral, namun tidak terbukti menurunkan jumlah folikel preantral dan berat ovarium tikus putih betina galur wistar. Dosis ekstrak etanol biji pepaya yang memiliki pengaruh paling besar terhadap jumlah folikel antral tikus putih betina pada dosis 0,3 mg/g BB.
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