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Background: Endometriosis pathogenesis is related to the inflammation shown by the secretion of pro-inflammatory mediators. This hypoxia condition can stimulate this condition. Objective: To investigate the effect of hyperbaric oxygen therapy (HBOT) on the inflammation reaction of endometriosis-induced mice. Materials and Methods: The animals were designated into 3 groups: I) the pre-test group, II) the post-test group receiving the HBOT, and III) the post-test group without HBOT. All groups were subjected to induction of endometriosis by xenotransplantation for 15 days. HBOT was given 30 min 3 times a day for 10 days. The evaluation of the HBOT effect was conducted by examining the endometrial tissue. The inflammation level was evaluated using the Klopfleisch semiquantitative scoring system (index remmele scale), whilst the expression of nuclear factor kappa (NFκB) beta was measured by immunohistochemical staining. Results: The results showed that group I demonstrated the highest level of inflammation degree (9.41 ± 1.99) compared to the post-test groups (group II: 1.60 ± 0.53; group III: 2.42 ± 0.53). The HBOT-groups was found to have the lowest inflammation level compared to the non-HBOT group (p = 0.020). The results demonstrated that HBOT lowered the peritoneal inflammation degree caused by the endometrial lesion in mice. NFκB expression on the post-test groups was significantly decreased, compared to the pre-test group (p ≤ 0.001), with a strong correlation between the NFκB expression and the peritoneal inflammation level (p ≤ 0.001, r = 0.670). Conclusion: HBOT significantly reduced the inflammation level on the endometrial lesion in mice, involving the NFκB pathway. Key words: Endometriosis, Hyperbaric oxygenation, Inflammation, Hypoxia, Mouse.

Dua masalah pokok yang menjadi perhatian para pakar di bidang pengetahuan kesehatan, khususnya para dokter, adalah pemahaman terhadap kesehatan serta mempertahankannya dan pemahaman terhadap penyakit serta terapinya. Pengetahuan dan pemahaman ilmu dasar menjadi kunci sukses terhadap kedua hal diatas. Terbitnya buku ajar Metabolisme dan Bioenergetika ini menjadi sangat penting dalam upaya meningkatkan pengetahuan pada ilmu dasar yang akan berkaitan erat pada banyak ilmu kedokteran lainnya. Pemaparan yang sangat ringkas dan sistematis membuat buku ajar ini mudah dimengerti dan dipahami sebagai salah satu sumber bacaan dalam pendidikan. Tentu keterkaitan ilmu ini dengan klinis sangat erat sehingga saya yakin meskipun penulis penyampaikan buku ini dipakai pada pembelajaran blok digestif, endokrin dan metabolism dasar, namun kenyataannya hampir semua cabang ilmu kedokteran membutuhkan pemahaman dasar yang diajarkan dalam buku ini. Bukan hanya bagi mahasiswa kedokteran semata melainkan juga seluruh mahasiswa dirumpun kesehatan. Terbitnya buku ini menjadi spesial sebagai karya civitas akademika FK Unsyiah di tengah Pandemi covid-19 yang secara fisik membatasi ruang gerak kita namun secara virtual justru semakin sibuk. Mudah-mudahan ini akan memacu staf pengajar lain serta ilmuan untuk melahirkan karya yang sama dalam ranah ilmu kesehatan yang berbeda demi kejayaan Ilmu Kedokteran dan Ilmu lainnya yang signifikan.

Objective: To evaluate morphological changes of breast cancer cell line MCF-7 following the development of acquired resistance towards cisplatin. Resistance towards anticancer agents still plays an important role in the breast cancer chemotherapy failure. Methods: The cisplatin resistant subline MCF-7/CisR was developed in-vitro by cultivating the parental cell line cisplatin-sensitive MCF-7 with raising concentration of cisplatin (from 0.01 to 2.3 µM) for four months. The cell morphology was observed by giemsa staining. Results: The resistance was shown by the increase of IC50 by 9 folds on MCF-7/CisR compared to the initial IC50 value of MCF-7. The change in cisplatin cytotoxic potency on the resistant cell line was accompanied by the morphological modification, including the enlargement of cell size, the increase of nucleus and cytoplasm ratio, and the increase of the number of microvesicular and cytoplasmic granules. Conclusions: This result has supported the underlying mechanism of cisplatin resistance, including the ability of the cells to decrease intracellular cisplatin concentration and repair DNA damage effects. Keywords: Drug resistance, human breast cancer, cisplatin, MCF-7 DOI: 10.15850/ijihs.v5n1.960

Objective : To investigate the effect of Phyllanthus niruri Linn (Euphorbiaceae) in the proliferation of human leukemic cells (MOLT-4 and K562). Methods: Phyllanthus niruri L ( P.niruri ) was macerated by using various solvents to obtain the crude extracts. Cytotoxicity of the extracts against MOLT-4 and K562 cells was tested using MTT assay to find the IC 50 value. To analyse cell cycle progression, cellular DNA was measured using propidium iodide (PI) staining. Apoptosis induction was evaluated using Annexin V-FITC and PI staining and analysed using FACSVerse flow cytometry. Finally, the expression of p53 on MOLT-4 and K562 cell lysate was measured by western blotting, to identify the possible mode of action of the anticancer activity. Results: P. niruri crude extracts demonstrated a potential anti-cancer effect towards MOLT-4 cells (IC 50 range was 42.21 ± 4.98 to 97.06 ± 18.29 µg/ml). However, against K562 cells, P.niruri extracts exhibited a lower inhibitory potency (the IC 50 was 120.19 ± 8.48 to 256.55 ± 26.22 µg/ml). The results showed the selectivity of the toxic effect of the extracts against MOLT-4 and K562. To evaluate the possible mechanism of action the anticancer effect, we evaluated P. niruri extract action in apoptosis induction and p53 expression. The results showed that methanol and hexane extract inhibited MOLT-4 cell progression from G1 to S-phase, indicating G1 cell arrest. Moreover, apoptotic cell population following treatment of MOLT-4 and K562 cells with methanol extract was markedly increased, showing morphological signs of apoptosis including membrane degradation and chromatin condensation. Furthermore, we found that there was an increase in p53 expression following MOLT-4 treatment with methanol extract , suggesting that p53 induction may be involved in cell apoptosis. Conclusions: The results indicated the involvement of p53 pathway in the mechanism of anti-cancer activity exerted by P. niruri extract on MOLT-4 cells . However, for cancer cells lacking P53 expression, such as K562 cells, apoptosis might take place via other pathways.