Yuliani, Fara Silvia
Department Of Pharmacology And Therapy, Faculty Of Medicine, Public Health And Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia

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Polyherbal formulation containing Saoropus androgynous, Trigonella foenum-graceum, and Moringa oleifera increased the expression of mRNA smooth muscle α-actin (ACTA2) and cytokeratin 14 (CK14) in lactating rats Fara Silvia Yuliani; Setyo Purwono; Ahmad Hamim Sadewa; Didik Setyo Heriyanto; Rahmaningsih Mara Sabirin; . Mustofa
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 51, No 2 (2019)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (244.749 KB) | DOI: 10.19106/JMedSci005102201902

Abstract

Polyherbal formulation (PHF) containing extracts of Sauropus androgynous, Trigonella foenum-graceum and Moringa oleifera has been proven can induce milk production in animal model. However, its molecular of action has not been elucidated, yet. This study aimed to investigate the effect of the PHF on the mRNA expressions of α-actin smooth muscle (ACTA2) and cytokeratin 14 (CK14) on the myoepithelial cells of the lactating rats mammary glands. Thirty female Wistar rats were divided into five groups with six of each. Group I was orally administered aquadest. Group II, III, and IV rats were orally administered the PHF at dose level of 26.25, 52.5, and 105 mg/kg once a day, for 15 days, respectively. Group V was orally administered 2.7 mg domperidone. On 16th day, rats were sacrificed. Mammary glands were isolated and processed for mRNA expression analysis using real-time polymerase chain reaction (qRT-PCR). The results demonstrated that the mRNA expression of ACTA2 and CK14 increased in dose-dependent manner in the groups of PHF. Significantly different between the Group III, IV, and V compared to Group I was observed (p < 0.05). However, there was no significantly different between Group IV and Group V (p>0.05). In conclusion, the PHF increases the mRNA expression of ACTA2 and CK14 on myoepithelial cells of the mammary glands on lactating rats.
Antifibrotic Effect of Ethanolic Extract of Nerium indicum Mill. Standardized 5α-Oleandrin on Keloid Fibroblasts Cells Mae Sri Hartati Wahyuningsih; Fara Silvia Yuliani; Dwiki Yuliya Rahmawati; Annisa Nurul Pratiwi
Majalah Obat Tradisional Vol 23, No 1 (2018)
Publisher : Faculty of Pharmacy, Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (418.022 KB) | DOI: 10.22146/mot.35116

Abstract

Keloid is a skin lesion caused by an abnormal proliferation of fibroblasts and the deposition of collagen in the wound healing process. Therapy for keloids is relatively limited and mostly has side effects. Recent studies show that 5α-oleandrin from N. indicum Mill. (N. indicum) has anti-keloid effect by inhibiting (proliferation, migration activity and TGF-β1 expression) keloid fibroblast. Further studies with N. indicum extract standardized 5α-oleandrin should be conducted to develop it as an anti-keloid agent by performing at proliferative effects, collagen accumulation, and keloid fibroblast migration. The antifibrotic activity of N. indicum extract on the proliferation of keloid fibroblasts was measured by MTT assay, whereas collagen deposits were observed by Sirius Red method. Observation of keloid fibroblast migration by scratch assay is according to Liang et al. (2009). Ethanol extract of N. indicum standardized 5α-oleandrin can inhibit the proliferation of keloid fibroblas with IC50 0.458 μg/mL, also inhibited collagen deposits with IC50 0.055 μg/mL at incubation for 72 hours. In incubation 48 hours after treatment with ethanol extract of 1.0 μg/mL occurred inhibition of migration significantly compared with control.
Expression of VEGF-A And COX-2 mRNA in non-steroidal anti-inflammatory drugs treated rat primary colonic fibroblast Andrew Limavanady; Jonathan J; Gloria Evita Thalia; Rasya Mayora; Ade Saputri; Rahmi Ayu Wijayaningsih; Eko Purnomo; Fara Silvia Yuliani; Woro Rukmi Pratiwi; Dwi Aris Agung Nugrahaningsih
Indonesian Journal of Pharmacology and Therapy Vol 1 No 1 (2020)
Publisher : Indonesian Pharmacologist Association or Ikatan Farmakologi Indonesia (IKAFI) and Faculty of Medicine, Public Health, and Nursing Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (253.945 KB) | DOI: 10.22146/ijpther.508

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) is often used to shorten recovery time after surgery, including after colon anastomosis surgery. Studies showed that NSAIDs might involve in the development of colon anastomotic leakage. However, the effect of NSAIDs in colon anastomosis leakage is still a subject of controversy. Studies indicated that selectivity of COX-2 might have a role in the deleterious effect of NSAIDs in colon anastomosis. Disruption of VEGF-A by NSAIDs also suspected to be the culprit in the development of anastomosis leakage during NSAIDs treatment. This study aimed to investigate the NSAIDs effect toward VEGF-A and COX-2 mRNA in rat primary colonic fibroblast. The in vitro study was conducted using fibroblast isolated from rat colon. The isolated fibroblast was divided into 4 groups of treatment i.e.controlgroup, acetaminophen group, metamizole group, and ketorolacgroup. After 48 h of treatment, the cell was harvested and the RNA was isolated. The expression of VEGF-A and COX-2 mRNA was conducted using semi-quantitative PCR(sq-PCR). Both VEGF-A and COX-2 were not expressed in untreated rat colon fibroblast. However, VEGF-A mRNA washighly expressed in the ketorolacgroup. Interestingly, COX-2 mRNA couldbe seen in the ketorolac and metamizole groups but not in the acetaminophen group. The COX-2 mRNA expression wasthe highest in ketorolac treated rat colon fibroblast. It can be concluded that the effect of various kinds of NSAIDs towards VEGF-A and COX-2 mRNA expression of colon fibroblasts is different. This condition is duetotheir different inhibitory selectivity towards COX-1 and COX2.