Objective: This study aimed to determine the cytoprotective potentials of citronella ( Cymbopogon nardus (L.) Rendl.) essential oil (CO) and lemongrass ( Cymbopogon citratus (DC.) Stapf) essential oil (LO). Methods: The essential oils from citronella and lemongrass were obtained by steam-water distillation, then analyzed using Gas Chromatography-Mass Spectrophotometry (GC-MS) to determine the chemical constituents. The antioxidant activity of CO and LO was compared using a total antioxidant capacity kit. The viability of normal kidney epithelial cells Vero and fibroblast NIH-3T3 as the cell models were tested using a trypan blue exclusion assay. The effect of cellular senescence inhibition on both cell models was measured using senescence-associated β-galactosidase (SA-β-gal) staining. The mechanism of action of CO and LO in the protection of cellular damage against doxorubicin was also confirmed through 2’,7’–dichlorofluorescin diacetate (DCFDA) staining to discover the ability to decrease reactive oxygen species (ROS) levels and a gelatin zymography assay to observe the activity of matrix metalloproteinases (MMPs). Results: The major marker components of CO and LO were citronellal and citral, respectively. Both oils showed low cytotoxic activity against Vero and NIH-3T3 cells, with IC 50 values of over 40 µg/mL. LO exhibited higher antioxidant capacity than CO, but there was no effect on the intracellular ROS level of both oils on Vero and NIH-3T3 cells. However, CO and LO decreased cellular senescence induced by doxorubicin exposure on both cells, as well as suppressed MMP-2 expression. Conclusion: Both CO and LO decrease the cellular senescence and MMP-2 expression with less cytotoxic effects on normal cells independently from their antioxidant capacities. The results were expected to support the use of CO and LO as tissue protective and anti-aging agents in maintaining the body’s cellular health against chemotherapeutics or cellular damaging agents.

Many chemotherapeutic agents cause various side effects, including nephrotoxicity. Doxorubicin, for example, increases the level of reactive oxygen species (ROS), leading to cell senescence in the kidneys. Cardamom essential oil (Amomum compactum Soland. ex Maton) contains compounds that exhibit antioxidant activity, such as 1.8-cineole, α-pinene, α-terpineol, and linalool. This study focused on exploring the potency of cardamom essential oil (CEO) as an anti-senescence induced by doxorubicin using Vero cells. CEO was obtained by steam distillation. The cytotoxic assay was carried out using trypan blue exclusion assay. We performed the 2',7'-dichlorodihydrofluorescein diacetate (DCFDA) staining and the senescence-associated beta-galactosidase (SA-β-gal) staining to measure the effect of CEO on intracellular ROS level and cell senescence, respectively. Analysis of the compounds with gas chromatography-mass spectrophotometry (GC-MS), revealed seven compounds with significant abundance, namely 1.8-cineole (50.82%), ß-pinene (12.43%), α-terpineol (8.50%), fenchone (4.10%), α-pinene (4.00%), sabinene (3.00%), and linalool (1.98%). The cytotoxicity assay of CEO on Vero cells showed an IC50 value of 178 μg/mL. Thus, the CEO is considered to be not cytotoxic and safe for normal kidney cells. Concentrations of 50 and 100 μg/mL reduced the senescence induced by doxorubicin. Therefore, the CEO has the potency as a nephroprotective agent in doxorubicin-induced senescence.

<p><span lang="EN-US">Mekanisme pertahanan sel kanker terhadap sistem imun tubuh merupakan ancaman bagi keberhasilan terapi kanker</span><span lang="EN-US">. Agen kemoterapi efektif dalam membantu proses eliminasi sel kanker, namun penggunaannya menginduksi imunosupresi. Ekstrak biji duwet (<em>Syzygium cumini</em> L. (Skeels.)) dan kandungan senyawanya dilaporkan memiliki berbagai aktivitas imunomodulator dan aktivitas antikanker. Namun, belum ada laporan yang mengulas potensi biji duwet sebagai agen imunomodulator pendamping kemoterapi kanker (ko-kemoterapi). Artikel ini disusun untuk mengulas potensi biji duwet sebagai imunomodulator pendamping kemoterapi. </span><span lang="EN-US">Berbagai literatur dari jurnal internasional dan sumber lain yang dipublikasikan mulai tahun 2005 ditelusuri dari <em>database</em> Pubmed, Scopus, Google<em> </em>Scholar, dan lainnya</span><span lang="EN-US">. Berdasarkan studi literatur, ekstrak dan senyawa kandungan biji duwet, yaitu asam galat dan mirisetin, dapat memodulasi sistem imun melalui berbagai jalur molekuler. Dapat disimpulkan bahwa biji duwet memiliki potensi untuk dikembangkan menjadi agen pendamping kemoterapi melalui aktivitas imunomodulatornya. </span><span lang="EN-US">Penelitian lebih lanjut pada model hewan uji kanker yang diberi ekstrak biji duwet dan kombinasinya dengan antikanker diperlukan untuk memvalidasi potensi tersebut.</span></p>

The treatment of glioblastoma multiforme (GBM) is challenging owing to its localization in the brain, the limited capacity of brain cells to repair, resistance to conventional therapy, and its aggressiveness. Curcumin has anticancer activity against aggressive cancers, such as leukemia, and GBM; however, its application is limited by its low solubility and bioavailability. Chemoprevention curcumin analog 1.1 (CCA-1.1), a curcumin analog, has better solubility and stability than those of curcumin. In this study, we explored potential targets of CCA-1.1 in GBM (PTCGs) by an integrated computational analysis and in vitro study. Predicted targets of CCA-1.1 obtained using various databases were subjected to comprehensive downstream analyses, including functional annotation, disease and drug association analyses, protein–protein interaction network analyses, analyses of genetic alterations, expression, and associations with survival and immune cell infiltration. Our integrative bioinformatics analysis revealed four candidate targets of CCA-1.1 in GBM: TP53, EGFR, AKT1, and CASP3. In addition to targeting specific proteins with regulatory effects in GBM, CCA-1.1 has the capacity to modulate the immunological milieu. Cytotoxicity of CCA-1.1 was lower than TMZ with an IC50 value of 9.8 μM compared to TMZ with an IC50 of 40 μM. mRNA sequencing revealed EGFR transcript variant 8 was upregulated, whereas EGFRvIII was downregulated in U87 cells after treatment with CCA-1.1. Furthermore, a molecular docking analysis suggested that CCA-1.1 inhibits EGFR with various mutations in GBM, which was confirmed using molecular dynamics simulation, wherein the binding between CCA-1.1 with the mutant EGFR L861Q was stable. For successful clinical translation, the effects of CCA-1.1 need to be confirmed in laboratory studies and clinical trials.

Jatropha (Jatropha curcas) is often used as biodiesel because of the oil content in its seeds. The production of jatropha oil generates a byproduct in the form of jatropha seed meal, which contains compounds with cytotoxic activity and phorbol esters, as co-carcinogens and tumor promoters. Meanwhile, metastasis is one of the characteristics of cancer where the cells spread to another tissue. This study aimed to determine the potential of jatropha seed meal as a chemoprevention agent, particularly an antimetastatic one, under bioinformatic study and molecular docking. Genecards and DAVID were performed to explore the protein involved in the metastatic process and its gene ontology. The prediction target protein was caught by SwissTargetPrediction. Jatropha seed meal showed the presence of isoamericanol A, myricetin, daidzein, gallic acid, and rutin. There are 11 prediction target proteins correlated to metastatic in extracellular matrix components. Then we were docked to a protein involved in metastasis, matrix metalloproteinase (MMP)-9 (PDB ID: 6ESM) using MOE software. The docking score determined the interaction properties. The docking analysis revealed that isoamericanol A, daidzein, and myricetin exhibited better binding affinity than native ligands and other compounds. Moreover, based on our literature study, the jatropha seed meal contains isoamericanol A, rutin, myricetin, daidzein, and gallic acid, which present anticancer properties by inhibition of cell invasion and migration, cell cycle arrest induction, and suppression of the MMP-9 activity. Overall, jatropha seed meal has potential as an antimetastatic agent. A comprehensive study is needed to explore the possibility of developing it as a supportive agent in combination with a chemotherapeutic agent.