Evaluation of Anti Carcinogenic Activity of Trifolium pratense on Oral Cancer Cell- An in vitro Study

Journal of Pharmaceutical Research International ◽

10.9734/jpri/2021/v33i47b33186 ◽

2021 ◽

pp. 800-806

Author(s):

V. A. Muralidharan ◽

R. V. Geetha

Keyword(s):

Oral Cancer ◽

Inhibitory Activity ◽

Trifolium Pratense ◽

Linear Regression Analysis ◽

Squamous Carcinoma ◽

Carcinoma Cells ◽

Carcinogenic Activity ◽

Squamous Carcinoma Cells ◽

Oral Squamous Carcinoma

Introduction: Trifolium pratense also known as the red clover is widely distributed in the tropics and in the subtropical regions. It is generally consumed in the form of tea by the northern states of India and some tribal people of Nepal and Bhutan. Studies reveal that it is rich in antioxidant and anti-inflammatory activity. It is due to the presence of unique isoflavones found in Trifolium pratense are Biohanin A and formononetin. Aim: The main aim of the study is to find out whether Trifolium pratense extract has antiproliferative activity against oral squamous carcinoma cells. Materials and Methods: The dried buds of Trifolium pratense flowers were purchased commercially and then powdered Then MTT assays was carried out to find out it’s inhibitory activity against oral carcinoma cells Results and Discussion: From the assay it is evident that it shows a potent inhibitory activity against oral squamous carcinoma cells. Linear regression analysis revealed that the IC50 was found to be at 53.13µg/ml which is higher than that of other species of this family. Conclusion: From the above study it is evident that Trifolium pratense has a very good inhibitory activity and hence can be used in the treatment of oral cancer.

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Modulation of growth and angiogenic potential of oral squamous carcinoma cells in vitro using salvianolic acid B

BMC Complementary and Alternative Medicine ◽

10.1186/1472-6882-11-54 ◽

2011 ◽

Vol 11 (1) ◽

Cited By ~ 26

Author(s):

Ya Yang ◽

Ping J Ge ◽

Long Jiang ◽

Feng L Li ◽

Qin Y Zhu

Keyword(s):

Squamous Carcinoma ◽

Carcinoma Cells ◽

Salvianolic Acid B ◽

Salvianolic Acid ◽

Angiogenic Potential ◽

Squamous Carcinoma Cells ◽

Oral Squamous Carcinoma

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Doxorubicin metabolism moderately attributes to putative toxicity in prodigiosin/doxorubicin synergism in vitro cells

Molecular and Cellular Biochemistry ◽

10.1007/s11010-020-03864-x ◽

2020 ◽

Vol 475 (1-2) ◽

pp. 119-126

Author(s):

Shian-Ren Lin ◽

Chun-Shu Lin ◽

Ching-Cheng Chen ◽

Feng-Jen Tseng ◽

Tsung-Jui Wu ◽

...

Keyword(s):

Squamous Carcinoma ◽

Human Kidney ◽

Carcinoma Cells ◽

Heart Cells ◽

Slight Reduction ◽

Normal Cells ◽

Squamous Carcinoma Cells ◽

Oral Squamous Carcinoma ◽

Metabolic Reduction

Abstract Doxorubicin (Dox) is a widely neoplasm chemotherapeutic drug with high incidences of cardiotoxicity. Prodigiosin (PG), a red bacterial pigment from Serratia marcescens, has been demonstrated to potentiate Dox’s cytotoxicity against oral squamous cell carcinoma cells through elevating Dox influx and identified as a Dox enhancer via PG-induced autophagy; however, toxicity of normal cell remains unclear. This study is conducted to evaluate putative cytotoxicity features of PG/Dox synergism in the liver, kidney, and heart cells and further elucidate whether PG augmented Dox’s effect via modulating Dox metabolism in normal cells. Murine hepatocytes FL83B, cardio-myoblast h9c2, and human kidney epithelial cells HK-2 were sequentially treated with PG and Dox by measuring cell viability, cell death characteristics, oxidative stress, Dox flux, and Dox metabolism. PG could slightly significant increase Dox cytotoxicity in all tested normal cells whose toxic alteration was less than that of oral squamous carcinoma cells. The augmentation of Dox cytotoxicity might be attributed to the increase of Dox-mediated ROS accumulation that might cause slight reduction of Dox influx and reduction of Dox metabolism. It was noteworthy to notice that sustained cytotoxicity appeared in normal cells after PG and Dox were removed. Taken together, moderately metabolic reduction of Dox might be ascribed to the mechanism of increase Dox cytotoxicity in PG-induced normal cells; nevertheless, the determination of PG/Dox dose with sustained cytotoxicity in normal cells needs to be comprehensively considered.

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