Chemoprevention with Aqueous Extract of Butea monosperma flowers results in normalization of nuclear morphometry and inhibition of a proliferation marker in liver tumors

Abstract

Butea monosperma (Lam.) (family: Fabaceae) popularly known as 'Palas' or 'fire of forest' has been used traditionally as a hepatoprotective agent. This study evaluated the hepatoprotective and antitumorigenic properties of the aqueous extract and butanol fractions of B. monosperma flowers in animal models. Dried flowers of B. monosperma were extracted with water and fractionated further using n-butanol. The hepatoprotective activity of the aqueous extract was initially confirmed in a carbon tetrachloride-induced liver damage model of rats. Oral administration of the aqueous extract produced a strong hepatoprotective effect similar to silymarin and normalized the serum levels of ALT, AST, bilirubin and triglyceride in rats. However, it did not affect the levels of glutathione and malondialdehyde which are oxidative stress markers in liver. Intraperitoneal administration of the aqueous extract in the X15-myc oncomice not only maintained liver architecture and nuclear morphometry but also down-regulated the serum VEGF levels. Immunohistochemical staining of liver sections with anti-Ribosomal protein S27a antibody showed post-treatment abolition of this proliferation marker from the tumor tissue. The butanol fractions, however, did not show antitumorigenic activity. Thus, the aqueous extract of B. monosperma flowers is not only hepatoprotective but also antitumorigenic by preserving the nuclear morphometry of the liver.

Combinatorial action of transcription factors orchestrates cell cycle‐dependent expression of the ribosomal protein genes and ribosome biogenesis

“…More recently, we reported the over‐expression of the RPS27a gene in an oncomouse model of hepatocellular carcinoma . The RPS27a levels decreased sharply following a chemopreventive intervention . Despite the emerging significance of RP genes in cancer development, cell cycle and cellular senescence, little is known about their regulatory control mechanisms.…”

The HBx protein of hepatitis B virus regulates the expression, intracellular distribution and functions of ribosomal protein S27a

“…This can be extrapolated from the fact that rapidly dividing hepatocytes in HCC tissue may have a higher metabolic rate than normal liver cells, and persistently high levels of RPS27a could contribute towards enhanced ribosome synthesis and protein turnover. Moreover, treatment of X15-myc mice with a plant extract bearing anti-cancer properties abolished the expression of RPS27a; these studies not only emphasized the involvement RPS27a in hepatocarcinogenesis, but also indicated a putative prognostic value of this protein (Mathan et al, 2011).…”

“…Subsequent studies suggested that some ribosomal proteins are overexpressed in HBV-associated human HCC tissues (Kim, 2006;Kim et al, 2004;Mathan et al, 2011). Enforced expression of ribosomal protein L36a is associated with increased cell proliferation and colony formation due to rapid cell cycling (Kim et al, 2004).…”

“…Further, heterozygous mutations in many ribosomal protein genes of zebrafish can lead to elevated cancer susceptibility, suggesting their role as tumour suppressors (Amsterdam et al, 2004). In the present study, we have investigated the physiological significance of overexpression of the ribosomal protein S27a in an HBx microenvironment of a transgenic mouse model of HCC (Mathan et al, 2011). …”

Litchi ( Litchi chinensis Sonn.) flower proanthocyanidin fraction exhibited protective efficacy to suppress nickel‐induced expression for vascular endothelial growth factor in HepG2 cells

“…The aqueous extract of Butea monosperma (Lam.) flower could reduce VEGF generation and inhibit proliferation of liver tumors of rats (Mathan et al, 2011). Resveratrol is a polyphenol, which could be found in grapes, various berries, peanuts, and many plant sources; it could suppress the proliferation for human ovarian and osteosarcoma cancer cells through inducing HIF-1ɑ degradation and downregulating VEGF expression (Cao, Fang, Xia, Shi, & Jiang, 2004).…”