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Paparan Pestisida Menginduksi Senesen Dini pada Mesenchymal Stem Cell In Vitro Adaninggar, Ascarti; Oktavya, Galuh; Putri, Raden Roro Risang Ayu Dewayani; Aprilianti, Suci Hari Utami; Nuriliani, Ardaning
Biota : Jurnal Ilmiah Ilmu-Ilmu Hayati Vol 9, No 1 (2024): February 2024
Publisher : Universitas Atma Jaya Yogyakarta

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24002/biota.v9i1.6340

Abstract

Pestisida merupakan senyawa kimia yang banyak digunakan sebagai pengendali hama pada aktivitas pertanian. Residu penggunaan pestisida ini dapat mengakibatkan polusi pada lingkungan perairan khususnya di sekitar lahan pertanian. Pestisida yang terakumulasi pada lingkungan perairan maupun hasil pertanian memberikan dampak buruk bagi manusia antara lain gangguan pada sistem organ, jaringan, perkembangan, dan pada tingkat sel mengarah ke senesen. Senesen merupakan suatu kondisi saat sel berhenti melakukan proliferasi. Sel yang mengalami senesen secara alami umumnya terjadi pada individu tua, sebagai respons terhadap pemendekan telomer. Senesen dini akibat paparan pestisida pada umumnya melibatkan mekanisme stres oksidatif, kerusakan DNA, dan disfungsi mitokondria. Senesen memicu penurunan fungsi organ yang mengakibatkan berbagai masalah kesehatan seperti kanker, osteoporosis, penyakit kardiovaskuler hingga demensia. Selain itu, senesen juga dapat menyebabkan berhentinya siklus sel punca antara lain pada mesenchymal stem cells (MSCs). Ulasan ini fokus membahas mekanisme senesen akibat paparan pestisida pada sel punca terutama MSCs. Metode yang digunakan yaitu koleksi data dan analisis dari jurnal terindeks Scopus dengan menggunakan VOSviewer. Berdasarkan hasil ulasan diketahui bahwa pestisida menginduksi senesen pada MSCs melalui jaras peningkatan konsentrasi ROS dalam sel dan penurunan aktivitas ALDH. Hal tersebut menyebabkan aktivasi p53, dan p21, yang kemudian akan menyebabkan hambatan pada CDK2 dan  pRB, berakibat pada  inaktivasi E2F serta induksi senesen. Senesen juga akan memberikan respons patofisiologis lain hingga efek tumorigenesis. 
Effect of Black Rice Bran ‘Sembada Hitam’ on T47D Breast Cancer Cells: Effect of Black rice bran on T47D Cios Conara , Flafiani; Oktavya, Galuh; Asih Purwestri, Yekti; Nuriliani, Ardaning
Journal of Tropical Life Science Vol. 13 No. 3 (2023)
Publisher : Journal of Tropical Life Science

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.11594/jtls.13.03.17

Abstract

Indonesians have a rich tradition of incorporating black rice into their diet as a functional food due to its high antioxidant content. This research investigates the effects of the ethanolic extract of "Sembada Hitam" black rice bran on T47D breast cancer cells, specifically its cytotoxic, cell growth, and apoptotic induction properties. The MTT assay method was used to evaluate the cytotoxicity of the black rice bran extract on T47D cells after 24 and 48 hours of incubation. The acridine orange/propidium iodide (AO/PI) dye double staining method was employed to assess the apoptosis-inducing properties of the extract. Additionally, a cell growth assay was conducted to evaluate the effect of the extract on cell growth, with observations recorded on days 0, 3, and 6. The results revealed that the ethanolic extract of black rice bran "Sembada Hitam," when administered at various concentrations ranging from 7.81 to 1000 µg/mL, did not exhibit cytotoxic effects on T47D cells during the 24 and 48 hours of incubation. The cell growth assay revealed that T47D cells treated with the ethanolic extract of "Sembada Hitam" black rice bran at concentrations of 250 and 500 µg/mL exhibited lower growth rates than the 1% DMSO group from the 3rd to 6th day after incubation. The ethanolic extract of "Sembada Hitam" at concentrations of 250, 500, and 1000 µg/mL resulted in cell death of 10.64 ± 2.98%, 9.99 ± 5.87%, and 5.84 ± 0.78%, respectively. In conclusion, this study found that the ethanolic extract of "Sembada Hitam" black rice bran did not demonstrate significant cytotoxic effects on T47D breast cancer cells and is, therefore, unlikely to be a suitable candidate for an anti-cancer agent.
Ethanolic Extract of Black Rice ‘Sembada Hitam’ Bran Did not Show Cytotoxic Effect on HeLa Cell (Cervical Cancer Cell Line) Nuriliani, Ardaning; Conara, Flafiani Cios; Oktavya, Galuh; Hidayah, Lailly Tsania Nur; Purwestri, Yekti Asih
Bioma : Berkala Ilmiah Biologi Vol. 25, No 1, Tahun 2023
Publisher : Departemen Biologi, Fakultas Sains dan Matematika, Universitas Diponegoro

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.14710/bioma.25.1.49-59

Abstract

Black rice (Oryza sativa L.) contains various phenolic compounds such as anthocyanins which act as antioxidants. Antioxidants inhibit cell proliferation and induced apoptosis of cancer cells as well as protect cells from damage that triggers cancer. 'Sembada Hitam' is a new cultivar of black rice in Indonesia that has not been studied for its anticancer potential. This study aimed to study the cytotoxic activity and apoptosis induction of the ethanolic extract of black rice (Oryza sativa L. 'Sembada Hitam') bran against HeLa cells. The method used was the cytotoxicity test with the MTT assay and the apoptosis test with the AO-PI double staining method. The test used various concentrations of black rice bran extract, DMSO as solvent control, and doxorubicin as a positive control for 24 and 48 hours. Data analysis was performed using one-way ANOVA (p = 0.05) followed by the Tukey HSD test. The results showed that ethanolic extract of black rice 'Sembada Hitam' bran has no cytotoxic activity against HeLa cells (p > 0.05). Moreover, extracts at the concentrations of 250 and 500 µg/mL only induced apoptosis of HeLa cells by 11.62 ± 0.50 and 11.49 ± 9.88% respectively. These results indicate that the ethanolic extract of black rice 'Sembada Hitam' bran has no potential to be developed as an agent for cervical cancer therapy.
Effect of Black Rice Bran ‘Sembada Hitam’ on T47D Breast Cancer Cells: Effect of Black rice bran on T47D Cios Conara , Flafiani; Oktavya, Galuh; Asih Purwestri, Yekti; Nuriliani, Ardaning
Journal of Tropical Life Science Vol. 13 No. 3 (2023)
Publisher : Journal of Tropical Life Science

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.11594/jtls.13.03.17

Abstract

Indonesians have a rich tradition of incorporating black rice into their diet as a functional food due to its high antioxidant content. This research investigates the effects of the ethanolic extract of "Sembada Hitam" black rice bran on T47D breast cancer cells, specifically its cytotoxic, cell growth, and apoptotic induction properties. The MTT assay method was used to evaluate the cytotoxicity of the black rice bran extract on T47D cells after 24 and 48 hours of incubation. The acridine orange/propidium iodide (AO/PI) dye double staining method was employed to assess the apoptosis-inducing properties of the extract. Additionally, a cell growth assay was conducted to evaluate the effect of the extract on cell growth, with observations recorded on days 0, 3, and 6. The results revealed that the ethanolic extract of black rice bran "Sembada Hitam," when administered at various concentrations ranging from 7.81 to 1000 µg/mL, did not exhibit cytotoxic effects on T47D cells during the 24 and 48 hours of incubation. The cell growth assay revealed that T47D cells treated with the ethanolic extract of "Sembada Hitam" black rice bran at concentrations of 250 and 500 µg/mL exhibited lower growth rates than the 1% DMSO group from the 3rd to 6th day after incubation. The ethanolic extract of "Sembada Hitam" at concentrations of 250, 500, and 1000 µg/mL resulted in cell death of 10.64 ± 2.98%, 9.99 ± 5.87%, and 5.84 ± 0.78%, respectively. In conclusion, this study found that the ethanolic extract of "Sembada Hitam" black rice bran did not demonstrate significant cytotoxic effects on T47D breast cancer cells and is, therefore, unlikely to be a suitable candidate for an anti-cancer agent.
Paparan Pestisida Menginduksi Senesen Dini pada Mesenchymal Stem Cell In Vitro Adaninggar, Ascarti; Oktavya, Galuh; Putri, Raden Roro Risang Ayu Dewayani; Aprilianti, Suci Hari Utami; Nuriliani, Ardaning
Biota : Jurnal Ilmiah Ilmu-Ilmu Hayati Vol 9, No 1 (2024): February 2024
Publisher : Universitas Atma Jaya Yogyakarta

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.24002/biota.v9i1.6340

Abstract

Pestisida merupakan senyawa kimia yang banyak digunakan sebagai pengendali hama pada aktivitas pertanian. Residu penggunaan pestisida ini dapat mengakibatkan polusi pada lingkungan perairan khususnya di sekitar lahan pertanian. Pestisida yang terakumulasi pada lingkungan perairan maupun hasil pertanian memberikan dampak buruk bagi manusia antara lain gangguan pada sistem organ, jaringan, perkembangan, dan pada tingkat sel mengarah ke senesen. Senesen merupakan suatu kondisi saat sel berhenti melakukan proliferasi. Sel yang mengalami senesen secara alami umumnya terjadi pada individu tua, sebagai respons terhadap pemendekan telomer. Senesen dini akibat paparan pestisida pada umumnya melibatkan mekanisme stres oksidatif, kerusakan DNA, dan disfungsi mitokondria. Senesen memicu penurunan fungsi organ yang mengakibatkan berbagai masalah kesehatan seperti kanker, osteoporosis, penyakit kardiovaskuler hingga demensia. Selain itu, senesen juga dapat menyebabkan berhentinya siklus sel punca antara lain pada mesenchymal stem cells (MSCs). Ulasan ini fokus membahas mekanisme senesen akibat paparan pestisida pada sel punca terutama MSCs. Metode yang digunakan yaitu koleksi data dan analisis dari jurnal terindeks Scopus dengan menggunakan VOSviewer. Berdasarkan hasil ulasan diketahui bahwa pestisida menginduksi senesen pada MSCs melalui jaras peningkatan konsentrasi ROS dalam sel dan penurunan aktivitas ALDH. Hal tersebut menyebabkan aktivasi p53, dan p21, yang kemudian akan menyebabkan hambatan pada CDK2 dan  pRB, berakibat pada  inaktivasi E2F serta induksi senesen. Senesen juga akan memberikan respons patofisiologis lain hingga efek tumorigenesis.