Silymarin is a phytochemical in the class of phenolic acids, found abundantly in peppermint, licorice, peanut, wheat, etc.
Health Benefits
1. Anti toxic effects
In the investigation of the effect of silymarin on doxorubicin-induced toxicity to the rat kidney, heart, and liver, found that the silymarin group received silymarin (100mg/kg) every other day. In the doxorubicin + silymarin group, silymarin
was injected ip at 100 mg/kg dose for 5 days before doxorubicin
administration (10 mg/kg, single ip injection) and then continued daily
thereafter until euthanization, Doxorubicin caused a significant
increase in serum NO levels compared to controls. Silymarin
pretreatment group lowered these. Histopathological and electron
microscopic examinations of kidney, heart, and liver sections showed
doxorubicin to cause myocardial and renal injury which was levv evident
in silymarin treated rats, according to "Protective Effects of Silymarin against Doxorubicin-induced Toxicity"by Cecen E, Dost T, Culhaci N, Karul A, Ergur B, Birincioglu M.(1)
2. Hepaprotective effects
In the investigation of the role of curcumin (CUR), silymarin
(SILY) and N-acetylcysteine (N-ACET) on hepatotoxicity by ATT drugs
using an in vitro model of human hepatocellular carcinoma cell line
(HepG2), found that that the presence of hepatoprotective drugs during
treatment of HepG2 cells with ATT drugs lowers the hepatotoxic effect
of the latter, according to "Protective effect of curcumin, silymarin and N-acetylcysteine on antitubercular drug-induced hepatotoxicity assessed in an in vitro model' by Singh M, Sasi P, Gupta VH, Rai G, Amarapurkar DN, Wangikar PP.(2)
3. Anti Cervical cancer
In the evaluation of the potential action of silymarin against cervical cancer and its mechanism of action, found that Silymarin induced apoptosis through the modulation of Bcl-2 family proteins and activation of caspase 3. Silymarin
also inhibited the phosphorylation of Akt with an increase in
expression of phosphatase and tensin homolog (PTEN). We also observed
that silymarin
suppressed C-33A cell invasion and wound-healing migration in a
concentration-dependent manner. Western-blot analysis showed that silymarin significantly inhibited the expression of matrix metalloproteinase-9 (MMP-9) in C-33A cells, according to "Silymarin Inhibits Cervical Cancer Cell Through an Increase of Phosphatase and Tensin Homolog" by Yu HC, Chen LJ, Cheng KC, Li YX, Yeh CH, Cheng JT.(3)
4. Anti cancers
In the review of the summarization of the recent investigations and mechanistic studies regarding possible molecular targets of silymarin for cancer prevention, found that the protective effects of silymarin and its major active constituent, silibinin, studied in various tissues, suggest a clinical application in cancer
patients as an adjunct to established therapies, to prevent or reduce
chemotherapy as well as radiotherapy-induced toxicity. This review
focuses on the chemistry and analogues of silymarin, multiple possible molecular mechanisms, in vitro as well as in vivo anti-cancer activities, and studies on human clinical trials, according to "Multitargeted therapy of cancer by silymarin" by Ramasamy K, Agarwal R.(4)
5. Prostate cancer
In the investigation of the stidy of three rat PCA cell lines, namely H-7, I-8, and I-26, were treated with silibinin or silymarin,
a crude silibinin-containing preparation, at various doses for varying
lengths of time. Cell growth and viability studies were carried out by
using hemocytometer and Trypan blue dye exclusion methods, found that
silibinin as well as silymarin
induce growth inhibition and apoptosis in rat PCA cells. These results
form a strong rationale for PCA prevention and therapeutic
intervention studies with silibinin and silymarin
in animal models, such as the MNU-testosterone rat PCA model, to
establish their efficacy and to further define their mechanisms of
action under in vivo conditions, according to "Antiproliferative and apoptotic effects of silibinin in rat prostate cancer cells" by Tyagi A, Bhatia N, Condon MS, Bosland MC, Agarwal C, Agarwal R.(5)
6. Liver cancer
In the assessment of the mechanisms involved in the growth inhibitory effect of silymarin, in humanhepatocellular carcinoma, found that Silymarin
inhibited population growth of the hepatocellular carcinoma cells in a
dose-dependent manner, and the percentage of apoptotic cells was
increased after treatment with 50 and 75 microg/ml silymarin for 24 h. Silymarin
treatment increased the proportion of cells with reduced DNA content
(sub-G(0)/G(1) or A(0) peak), indicative of apoptosis with loss of cells
in the G(1) phase. Silymarin
also decreased mitochondrial transmembrane potential of the cells,
thereby increasing levels of cytosolic cytochrome c while up-regulating
expression of pro-apoptotic proteins (such as p53, Bax, APAF-1 and
caspase-3) with concomitant decrease in anti-apoptotic proteins (Bcl-2
and survivin) and proliferation-associated proteins (beta-catenin,
cyclin D1, c-Myc and PCNA), according to "Silymarin inhibited proliferation and induced apoptosis in hepatic cancer cells" by Ramakrishnan G, Lo Muzio L, Elinos-Báez CM, Jagan S, Augustine TA, Kamaraj S, Anandakumar P, Devaki T.(6)
7. Bladder cancer
In
the searching the underlying mechanisms and examining the intravesical
efficacy of silibinin, a natural flavonoid in the prevention and
treatment of bladder cancer. Human bladder carcinoma cell line 5637, which has the same molecular features of high-risk superficial bladder cancer,
was used as the model system in vitro and in vivo, found that oral
silibinin suppressed the growth of 5637 xenografts, which was
accompanied with the activation of caspase-3, downregulation of
survivin, and increased translocation of AIF. Furthermore, intravesical
silibinin effectively inhibited the carcinogenesis and progression of
bladder cancer
in rats initiated by MNU by reducing the incidence of superficial and
invasive bladder lesions without any side effects, which was accompanied
with proapoptotic effects, according to "Chemopreventive and chemotherapeutic effects of intravesical silibinin against bladder cancer by acting on mitochondria" by Zeng J, Sun Y, Wu K, Li L, Zhang G, Yang Z, Wang Z, Zhang D, Xue Y, Chen Y, Zhu G, Wang X, He D.(7)
8. Antioxidants and anti cancers
In the study of the effect of three natural antioxidants curcumin, silymarin
and acteoside on AP9-cd (standardized lignan composition from Cedrus
deodara) induced cytotoxicity in human leukemia HL-60 cells, found that
out of the three antioxidants, curcumin was found to be more potent than
acteoside and silymarin
in terms of enhancing the apoptotic potential of AP9-cd. These results
propose an important role of natural antioxidant as adjuvant to
enhance the anticancer potential of AP9-cd and more likely other
anti-neoplastic therapeutics, according to "Natural
antioxidants synergistically enhance the anticancer potential of
AP9-cd, a novel lignan composition from Cedrus deodara in human
leukemia HL-60 cells" by Saxena A, Saxena AK, Singh J, Bhushan S.(8)
9. Antimetastatic effects
In
the investigation of Silibinin, a popular dietary supplement isolated
from milk thistle seed extracts against a variety of cancers, found
that detailed mechanistic analyses revealed that silibinin targets
signaling molecules involved in the regulation of
epithelial-to-mesenchymal transition, proteases activation, adhesion,
motility, invasiveness as well as the supportive tumor-microenvironment
components, thereby inhibiting metastasis. Overall, the long history
of human use, remarkable nontoxicity, and preclinical efficacy strongly
favor the clinical use of silibinin against advanced metastatic
cancers, according to "Antimetastatic efficacy of silibinin: molecular mechanisms and therapeutic potential against cancer" by Deep G, Agarwal R.(9)
10. Gastric cancer
In the determination of the effect of silibinin on TNF-alpha-induced MMP-9 expression in gastric cancer cell lines. MMP-9 mRNA and protein expression was dose-dependently increased by TNF-alpha in SNU216 and SNU668 gastric cancer
cells, found that the expression of MMP-9 was significantly increased
by CA-MEK overexpression, but not by CA-Akt overexpression. Taken
together, we suggest that silibinin down-regulates TNF-alpha- induced
MMP-9 expression through inhibition of the MEK/ERK pathway in gastric cancer cells, according to "Silibinin suppresses TNF-alpha-induced MMP-9 expression in gastric cancer cells through inhibition of the MAPK pathway" by Kim S, Choi MG, Lee HS, Lee SK, Kim SH, Kim WW, Hur SM, Kim JH, Choe JH, Nam SJ, Yang JH, Kim S, Lee JE, Kim JS.(10)
11. Etc.
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/22320977
(2) http://www.ncbi.nlm.nih.gov/pubmed/22318308
(3) http://www.ncbi.nlm.nih.gov/pubmed/22016029
(4) http://www.ncbi.nlm.nih.gov/pubmed/18472213
(5) http://www.ncbi.nlm.nih.gov/pubmed/12386921
(6) http://www.ncbi.nlm.nih.gov/pubmed/19317806
(7) http://www.ncbi.nlm.nih.gov/pubmed/21220495
(8) http://www.ncbi.nlm.nih.gov/pubmed/20932957
(9) http://www.ncbi.nlm.nih.gov/pubmed/20714788
(10) http://www.ncbi.nlm.nih.gov/pubmed/19924065
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