ABSTRAKJahe merah (Zingiber officinalle var. Amarum) merupakan salah satu tumbuhan yang banyak digunakan sebagai bumbu makanan sehari-hari dan juga berkhasiat sebagai obat tradisional untuk mengobati berbagai penyakit termasuk asam urat. Penelitian ini bertujuan untuk menguji aktifitas biologi dari jahe merah dan mengisolasi dan mengidentifikasi senyawa bioaktif yang tekandung di dalam ekstraknya. Berdasarkan penelitian yang dilakukan terhadap ekstrak etanol jahe merah memperlihatkan kemampuannya dalam menurunkan asam urat pada kelinci yang diinduksi dengan kalium bromat (KBrO3) pada konsentrasi 0,6 b/v yang diamati pada 1 dan 3 jam setelah diinduksi dan dibandingkan dengan allopurinol yang digunakan sebagai positif kontrolnya. Ekstrak etanol jahe merah juga memperlihatkan hubungan konsentrasi dengan penurunan asam urat pada kelinci. Isolasi senyawa bioaktif dalam tanaman ini telah dilakukan dengan menggunakan metode kromatografi dan identifikasi stukturnya didasarkan pada analisis data spektrofotometri dan NMR. Berdasarkan data spectra yang diperoleh terhadap senyawa yang paling dominan yang berhasil diisolasi dan diidentifikasi adalah senyawa 6-gingerol. Hal ini menunjukkan bahwa ekstrak etanol jahe merah memiliki aktifitas dalam menurunkan kadar asam urat dengan senyawa utama 6-gingerol.

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Accumulating evidence suggests that inflammation is linked to multiple pathological processes and induces cellular and molecular damage through the activation of inflammatory signaling pathways, including the NF-κB pathway. The aim of the present study was to identify natural anti-inflammatory products that can target NF-κB activity, in order to establish a novel therapeutic approach for inflammatory diseases. Using a 4T1 breast cancer cell line that expresses the firefly luciferase gene under the control of an NF-κB response element, 112 natural products were tested for their anti-inflammatory properties. Sohakuhi (Morus alba Linn. bark) extract was observed to strongly suppress NF-κB activity without affecting cell viability. To further examine the anti-inflammatory effect of Sohakuhi, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cellular damage of human HaCaT keratinocytes was evaluated. While TRAIL triggered the phosphorylation of the p65 subunit of NF-κB, leading to cellular damage in HaCaT cells, treatment with Sohakuhi extract protected HaCaT cells against TRAIL-induced cellular damage. Moreover, Sohakuhi treatment also upregulated the anti-apoptotic proteins Bcl-xL and Bcl-2. Importantly, through chemical fractionation of Sohakuhi extract, moracin O and P were confirmed to mediate its anti-inflammatory effects. Collectively, the present results indicated that Sohakuhi and moracin may represent potential candidates for the development of novel anti-inflammatory drugs.

The most common type of skin cancer is melanoma. While significant advances in chemotherapy have occurred in a few instances, only marginal progress has been made in treating metastatic melanoma. Natural medicine has traditionally been used to treat various illnesses, including cancer. The purpose of this study was to identify the active compound in Kaempferia galanga, which could be used to treat melanoma as an anti-metastasis and chemosensitizer agent. The active compound in K. galanga was isolated and identified using chromatography and spectroscopy techniques, and given six compounds. Inhibitory activity on NFκB activation and cell viability was determined using reporter assay methods. Among the isolated compounds, ethyl p-methoxycinnamate (EPMC) demonstrated potent NFκB inhibitory activity against melanoma cell B16F10- NFκB Luc2 with an IC50 of 88.7 μM. Further investigation was conducted by evaluating the anti-metastasis effect of EPMC in vitro by using wound-healing assays, invasion tests, and molecular mechanism assays using Western blotting. NFκB has been implicated in tumorigenesis through the PI3K/Akt/NFκB pathway. The results of this study indicated that EPMCs act as inhibitors of p38 and thereby Akt phosphorylation inhibitors at serine 473, inhibiting NFκB-dependent transcription. Further analysis with paclitaxel demonstrated that the combinations could sensitize to apoptosis in response to well-known chemotherapy agents. Additional studies were conducted using the human melanoma cancer cell line SK-Mel 28. Along with the induction of apoptosis, we observed an increase in p-γH2AX expression (a molecular marker for double strand breaks in DNA damage) in response to treatment with paclitaxel and EPMC. The result showed EPMC to be a potential, viable adjuvant for improving the clinical efficacy of anti-metastatic and cancer chemotherapy.