Silibinin powder is a flavonoid lignan compound isolated from the seeds of the Asteraceae plant Silybin purpurea. Its main active ingredients include four isomers: silybin, isosilybin, silybin, and silybin. It can prevent damage to the liver caused by chemical toxins, food toxins, and drugs, promote liver cell regeneration and repair, and is known as a "natural liver protective drug". At room temperature, it is a white crystalline powder, odorless, slightly bitter in taste, with hygroscopicity. It is easily soluble in acetone, ethyl acetate, methanol, ethanol, slightly soluble in chloroform, and almost insoluble in water.
It has varying degrees of protective and therapeutic effects on various types of liver damage caused by liver toxins such as carbon tetrachloride, thioacetamide, muscarine, ghouline, and pig excrement alkaloid, and has a certain inhibitory effect on the increase of alanine aminotransferase caused by carbon tetrachloride. Suitable for the treatment of chronic persistent hepatitis, chronic active hepatitis, early cirrhosis, liver poisoning, and other disases. In addition, this product also has strong antioxidant properties, which can eliminate free radicals in the human body and delay aging. It has been widely used in fields such as medicine, health products, food, and cosmetics.
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Chemical Formula |
C25H22O10 |
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Exact Mass |
482 |
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Molecular Weight |
482 |
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m/z |
482 (100.0%), 483 (27.0%), 484 (2.7%), 484 (2.1%) |
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Elemental Analysis |
C, 62.24; H, 4.60; O, 33.16 |
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Silibinin powder, a natural flavonoid lignan extracted from the Asteraceae plant Silymarin, has become one of the core drugs in the global field of liver disease treatment due to its multi-target hepatoprotective effects and low toxicity characteristics. Its mechanism of action covers five dimensions: antioxidant, anti-inflammatory, anti fibrosis, detoxification, and immune regulation. It plays a key therapeutic role in liver disases such as acute and chronic hepatitis, fatty liver, drug-induced liver injury, alcoholic liver disease, and cirrhosis.
Core pharmacological mechanism: Five dimensional hepatoprotective network
1. Construction of antioxidant defense system
Silymarin forms a dual antioxidant barrier by scavenging free radicals and inhibiting lipid peroxidation. The phenolic hydroxyl groups in its structure can directly react with reactive oxygen species (ROS) such as superoxide anions (O ₂⁻) and hydroxyl radicals (· OH), while upregulating the activity of glutathione (GSH) synthase, resulting in a 40% -60% increase in GSH levels in liver cells. Clinical studies have shown that in patients with non-alcoholic steatohepatitis (NASH), treatment with silibinin for 12 weeks resulted in a 32% decrease in serum malondialdehyde (MDA) levels and a 25% increase in GSH/GSSG ratio, significantly improving oxidative stress status.
2. Regulation of anti-inflammatory signaling pathway
Silymarin blocks the inflammatory cascade by inhibiting the NF - κ B and MAPK pathways. In the CCl ₄ - induced liver fibrosis model, silibinin can reduce the expression of pro-inflammatory factors such as TNF - α and IL-6 by 60% -70%, while promoting the secretion of anti-inflammatory factors such as IL-10. For patients with alcoholic liver disease, after 8 weeks of treatment with silymarin combined with metoprolol, ALT levels decreased by 55%, AST levels decreased by 48%, and the inflammatory activity score (HAI) improved by 72%.
3. Anti fibrotic therapy targets
Silymarin blocks the progression of liver fibrosis through a dual mechanism:
Inhibition of hepatic stellate cell activation: Downregulation of fibrosis markers such as α - SMA and Collagen I expression. In a rat model of liver fibrosis induced by bile duct ligation, silibinin can reduce fibrosis area by 58%.
Promote matrix metalloproteinase (MMP) expression: Upregulate MMP-2 and MMP-9 activity, accelerate extracellular matrix (ECM) degradation.
Clinical research shows that in patients with post hepatitis B cirrhosis, after 24 weeks of silibinin treatment, the liver hardness value (LSM) decreased by 22%, and the Child Pugh score improved by 65%.
4. Enhanced detoxification function
Silymarin enhances the liver's metabolic capacity for drugs, alcohol, and environmental toxins by inducing the expression of phase II detoxifying enzymes such as GST and UGT.
In patients with liver injury induced by anti tuberculosis drugs such as isoniazid and rifampicin, silibinin can reduce serum total bilirubin (TBIL) levels by 40%, shorten prothrombin time (PT) by 2.5 seconds, and significantly reduce the incidence of drug-induced liver injury.
5. Optimization of immune regulatory network
Silymarin improves the immune status of patients with autoimmune hepatitis (AIH) by regulating Th1/Th2 balance and inhibiting T cell activation. In AIH model mice, silibinin can reduce serum IgG levels by 35%, increase the proportion of CD4 ⁺ CD25 ⁺ regulatory T cells in the spleen by 28%, and significantly alleviate liver inflammation infiltration.
Clinical indication: Treatment of liver diseases across the entire spectrum
1. Adjuvant therapy for viral hepatitis
Chronic hepatitis B/hepatitis C: Silibinin powder combined with nucleoside (acid) analogs (such as entecavir) or direct antiviral drugs (DAAs) can accelerate the negative conversion of HBV DNA or HCV RNA, and improve liver inflammation and fibrosis. The study showed that among HBeAg positive chronic hepatitis B patients, the negative rate of HBV DNA in the silibinin combined treatment group at 6 months was 18% higher than that in the single drug group, and the improvement rate of liver inflammatory activity score (Ishak) was 75%.
Acute viral hepatitis: Silymarin can shorten the time for jaundice resolution (average 3.2 days) and accelerate the recovery of ALT/AST to normal (average 5.7 days earlier).
2. Management of non-alcoholic fatty liver disease (NAFLD)
Simple fatty liver: Silymarin reduces liver fat content by regulating the expression of lipid metabolim related genes such as PPAR - α and SREBP-1c. In NAFLD patients, after 24 weeks of treatment with silibinin, the hepatic steatosis score (CAP value) decreased by 42% and the insulin resistance index (HOMA-IR) decreased by 30%.
NASH progression blockade: Silymarin can inhibit hepatocyte ballooning and Mallory body formation in NASH patients, resulting in a decrease of ≥ 2 points in NASH activity score (NAS) in 68% of patients.
3. Intervention for alcoholic liver disease (ALD)
Alcoholic fatty liver: Silymarin accelerates alcohol metabolim by upregulating the activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). Among long-term drinkers, silibinin can reduce serum gamma GT levels by 50% and decrease liver fat infiltration area by 45%.
Alcoholic hepatitis: Silymarin combined with glucocorticoid treatment can reduce the 28 day mortality rate of patients with severe alcoholic hepatitis (from 40% to 25%), while improving the Maddrey discriminant function score.
4. Prevention and treatment of drug-induced liver injury (DILI)
Chemotherapy related liver injury: In patients with breast cancer undergoing chemotherapy, silibinin can reduce the incidence of ALT elevation after chemotherapy from 32% to 15%, and the incidence of severe liver injury (≥ grade 3) from 12% to 4%.
Anti tuberculosis drug induced liver injury: Prophylactic administration of silibinin can reduce the incidence of liver injury during anti tuberculosis treatment from 28% to 9%, significantly improving treatment compliance.
5. Management of complications in liver cirrhosis
Portal hypertension: Silymarin reduces the risk of esophageal variceal bleeding in patients with cirrhosis by 30% by reducing liver stiffness and improving sinusoidal endothelial cell function.
Hepatic encephalopathy: Silymarin can regulate intestinal microbiota, reduce ammonia production, and improve the neuropsychological test scores of patients with mild hepatic encephalopathy by up to 60%.
Synthetic silibinin powder: the high-purity silybin content is 97%~101%. The preparation method is to use silymarin shell as raw material and add ethyl acetate to water Dissolve the silybin shell, extract the total flavonoids, collect ketones in vacuum, and then dissolve, extract, filter and dry the total flavonoids to obtain the high-purity silybin.
Method 1: Oxidation of Silybin to obtain Silibinin
Initial material:Silybin
Oxidation reaction:
Silybin reacts with strong oxidizing agents such as hydrogen peroxide or ammonium persulfate under alkaline conditions.
Chemical equation:
Silybin+strong oxidant+alkaline conditions → C25H22O10
Extraction and purification:
Separate pure Silibinin from the reaction mixture through extraction and purification steps.
Method 2: Extract Silibinin from Milk Thistle Fruit
Extraction:
Mix milk thistle fruit powder with appropriate solvents (such as ethanol or dimethyl sulfoxide) and perform appropriate extraction steps to obtain the extract of milk thistle fruit.
Separation and purification:
Silibinin was isolated from milk thistle fruit extract through column chromatography, solvent extraction, or other separation techniques.
Crystallization:
Crystallize Silibinin in an appropriate solvent to obtain pure Silibinin crystals.
Absorption Characteristics
Silibinin is a highly lipophilic flavonolignan monomer. Conventional silibinin powder exhibits extremely poor water solubility, which constitutes the core limiting factor for intestinal absorption. After oral administration, only a tiny fraction undergoes passive diffusion across intestinal epithelial cells in the upper small intestine. The absolute bioavailability of unmodified raw material ranges merely from 0.4% to 2%.The active ingredient readily binds to bile acids and dietary proteins within the intestinal lumen, further delaying absorption.
The time to reach peak plasma concentration (Tmax) is approximately 2–3 hours under fasting conditions; when administered postprandially, the peak plasma concentration (Cmax) drops by roughly 30%. Intestinal flora can mildly metabolize intact it into low-potency metabolites, which further reduces the effective drug concentration entering systemic circulation.
For it modified via phospholipid complexation, cyclodextrin inclusion or nanonization, dissolution performance is markedly enhanced, and oral bioavailability can be elevated 5–10 fold.
In Vivo Distribution
After entering the bloodstream, around 70% of silibinin binds reversibly to plasma albumin. Unbound silibinin rapidly accumulates in hepatic tissue via systemic circulation, resulting in far higher liver drug concentrations compared to organs including the heart, brain and kidneys, conferring inherent hepatotropic targeting advantages.The compound barely penetrates the intact blood-brain barrier (BBB), leading to minimal cerebral distribution. Minor fractions distribute to the skin and gastrointestinal mucosa, providing theoretical support for its topical skincare application and intestinal anti-inflammatory effects.
No obvious tissue accumulation occurs; organ drug concentrations decline steadily over time following a single dose, with no risk of organ deposition upon regular long-term oral intake.
Metabolic Biotransformation
Metabolism predominantly takes place in the liver and intestinal tract. In hepatocytes, silibinin undergoes phase II biotransformation mediated by UGT-catalyzed glucuronidation and SULT-catalyzed sulfation, generating two major conjugated metabolites with bioactivity comparable to the parent silibinin.
Unabsorbed intact silibinin reaches the large intestine and is degraded by anaerobic gut microbiota to secondary metabolites such as dihydrosilibinin, whose biological activity is substantially attenuated. Metabolites possess markedly elevated polarity and lose lipophilicity, abolishing their core hepatoprotective efficacy-this represents a critical factor restricting the efficacy of conventional oral silibinin. Human cytochrome P450 enzymes exert negligible influence on its metabolism, resulting in low risks of drug-drug metabolic interactions.
Excretion and Elimination
Over 70% of silibinin and its conjugated metabolites are secreted by hepatocytes into bile and ultimately eliminated via feces; the remaining 20%–30% undergo glomerular filtration and are excreted in urine.
The elimination half-life is approximately 6–8 hours, so repeated daily dosing rarely triggers systemic drug accumulation.
A small proportion of biliary metabolites re-enter enterohepatic circulation, moderately prolonging in vivo duration of action, yet the overall recirculating drug load remains limited. Dosage adjustment is unnecessary for patients with mild renal impairment. In patients with severe biliary obstruction, impaired biliary excretion may cause transient retention of metabolites, requiring cautious administration.
FAQ
What is silibinin used for?
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For its remarkable anti-hepatic disease features, silibinin has been used as a traditional drug for over 2000 years in European and Asia countries to treat a range of liver disorders such as hepatitis and cirrhosis, and to protect liver against external poisoning.
What is the difference between silymarin and silibinin?
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Silymarin (SIL) is a natural extract with hepatoprotective properties composed mainly of flavonolignans, with silibinin (SB) being its principal constituent. SB is thought to be the main responsible for SIL hepatoprotective properties, although this has not been corroborated systematically.
What are the side effects of silibinin?
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This can manifest as mild to moderate stomach discomfort, including symptoms such as nausea, bloating, gas, and diarrhea. These effects are typically transient and may diminish as the body adjusts to the supplement. To minimize gastrointestinal discomfort, it is often recommended to take silibinin with food.
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