Database Query Results : Baicalein, , hepatoP

Ba, Baicalein: Click to Expand ⟱
Features:
Baicalein is a flavone, a type of flavonoid, originally isolated from the roots of Scutellaria baicalensis and Scutellaria lateriflora. It is also a constituent of Oroxylum indicum and thyme.
Baicalein, a flavonoid found in several medicinal plants (notably Scutellaria baicalensis), has been investigated for its anticancer properties. Its activities involve modulation of multiple cellular pathways, including those that regulate cell proliferation, apoptosis, metastasis, and oxidative stress. Here are some of the key pathways and mechanisms implicated in its anticancer effects:
-Apoptosis and Cell Cycle Regulation
-Reactive Oxygen Species ROS↑ Generation and Oxidative Stress (Context and dose dependent)
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspase-3↑, Caspase-9↑, DNA damage↑,
-Baicalein’s effects on ROS are context-dependent. In some cancer cells, it promotes ROS production to a degree that overwhelms the antioxidant defenses. Elevated ROS levels can damage cellular components and promote apoptosis, essentially tipping the balance toward cell death.
-Conversely, in normal cells, baicalein may exhibit antioxidant properties and reduce ROS↓ under conditions of oxidative stress, highlighting its dual role.
- May Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓, HO-1↓
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑, HO-1↑,
-MAPK, ERK Pathway:
-PI3K/Akt Pathway: Inhibition of the PI3K, Akt pathway by baicalein.
-NF-κB Pathway: Baicalein can inhibit
-Inhibition of Metastasis and Invasion: Baicalein can downregulate MMPs, MMP2, MMP9
-Angiogenesis Suppression: VEGF
-Baicalein is a well-known inhibitor of 12-lipoxygenase
-inhibitor of Glycolysis↓ and HIF-1α↓, PKM2↓, cMyc↓, PDK1↓, GLUT1↓, LDHA↓, HK2↓
- promoting PTEN
-chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, neuroprotective, Cognitive, Renoprotection, Hepatoprotective, cardioProtective,
- Selectivity: Cancer Cells vs Normal Cells
-low bioavailability but liposomal may improve bioavailability

In summary, baicalein affects cancer cells by modulating multiple pathways—promoting apoptosis, causing cell cycle arrest, generating or modulating ROS levels, inhibiting survival and proliferative signaling (such as MAPK, PI3K/Akt, and NF-κB pathways), and reducing angiogenesis and metastasis.

Many animal studies, doses have been reported in the range of approximately 10 to 200 mg/kg body weight.
For example, some studies exploring anticancer or anti-inflammatory effects in rodent models have used doses around 50–100 mg/kg.
However, these doses do not directly translate to human dosages.
Some human studies or formulations (where they are used as nutraceuticals or supplements) may suggest dosing in the range of a few hundred milligrams per day of the extract, but it is often not standardized to a specific amount of baicalein or baicalin.
-mix with oil?

-ic50 cancer cells 10-30uM, normal cells 50-100uM
-Animal studies, 10 to 100 mg/kg.
-Reported to induce apoptosis, cause cell cycle arrest, inhibit angiogenesis, and modulate various signaling pathways (e.g., STAT3, NF-κB, MAPK).

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS (tumor-selective oxidative stress) ↑ ROS (P→R); can progress to cytotoxic stress (G) ↔ or ↓ ROS under oxidative challenge (R→G) P, R, G Stress amplifier Baicalein can act as a pro-oxidant in many tumor contexts while behaving as an antioxidant in non-malignant or stressed-normal contexts; net direction is dose/model dependent.
2 Mitochondrial membrane potential (ΔΨm) / mitochondrial integrity ↓ ΔΨm (R); downstream commitment to death programs (G) ↔ preserved R, G Mitochondrial failure threshold Loss of ΔΨm is a common convergence point after sustained oxidative / stress signaling and precedes cytochrome-c release and caspase activation.
3 Cytochrome-c release → Caspase-9/3 activation (intrinsic apoptosis) ↑ Cyt-c, ↑ Caspase-9, ↑ Caspase-3 (G) ↔ minimal activation G Apoptosis execution Typically appears after upstream redox/mitochondrial stress has crossed a commitment threshold; aligns with intrinsic apoptotic signaling.
4 ER stress / UPR + Ca²⁺ dysregulation ↑ ER stress, ↑ Ca²⁺ signaling (R→G) ↔ buffered homeostasis R, G Stress-to-death coupling ER stress and Ca²⁺ transfer can amplify mitochondrial dysfunction; sustained stress favors pro-death UPR signaling.
5 DNA damage / oxidative injury markers ↑ DNA damage (R→G) ↔ or efficiently repaired (G) R, G Checkpoint stress Often interpreted as a downstream consequence of sustained ROS and impaired redox buffering rather than a primary “direct DNA” effect.
6 Antioxidant defense balance (NRF2, GSH, HO-1; SOD/Catalase) ↓ NRF2 / ↓ GSH / ↓ HO-1 (R→G) ↑ NRF2 / ↑ GSH / ↑ HO-1; ↑ SOD/Catalase (R→G) R, G Selectivity gate Reported divergence suggests tumors may fail to mount sufficient antioxidant adaptation while normal cells compensate; magnitude varies by model and baseline redox state.
7 PI3K → AKT survival axis ↓ PI3K/AKT signaling (R→G) ↔ limited effect R, G Survival suppression Reduced pro-survival signaling increases vulnerability to stress-induced apoptosis and can contribute to cell-cycle effects.
8 MAPK / ERK pathway modulation MAPK/ERK modulation (often ↓ ERK tone) (P→R→G) ↔ context-dependent P, R, G Signal re-wiring MAPK readouts often shift early (phosphorylation) and can later reshape gene programs; direction can vary across tumor types and dosing.
9 NF-κB signaling ↓ NF-κB activity (R→G) ↔ R, G Anti-survival / anti-inflammatory transcription NF-κB suppression reduces pro-survival stress responses and inflammatory tone; may support chemo-/radio-sensitization in some settings.
10 Glycolysis / hypoxia program (HIF-1α; PKM2, PDK1, GLUT1, LDHA, HK2; c-Myc) ↓ Glycolysis and associated nodes; ↓ HIF-1α / ↓ c-Myc (G) ↔ G Metabolic constraint Best interpreted as a gene-regulatory / adaptation-level effect; specific node changes are model dependent even when “glycolysis suppression” is observed.
11 Invasion / metastasis programs (MMP2/MMP9 and related MMPs) ↓ MMP2 / ↓ MMP9 (G) ↔ G Anti-invasive phenotype Usually reflected in later expression/phenotype assays (migration/invasion) rather than immediate signaling events.
12 Angiogenesis signaling (VEGF) ↓ VEGF (G) ↔ G Anti-angiogenic support Typically manifests as reduced VEGF expression/secretion and downstream angiogenic behavior over longer observation windows.
13 12-lipoxygenase (12-LOX / 12/15-LOX) inhibition ↓ 12-LOX activity (P→R) ↔ P, R Direct enzymatic target Often treated as a relatively “direct” biochemical interaction compared with downstream transcriptional programs.
14 PTEN (tumor suppressor axis) ↑ PTEN (G) ↔ G Brake on PI3K/AKT PTEN increases are generally best treated as gene-regulatory/adaptation-level outcomes that reinforce PI3K/AKT suppression.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (primary/physical–chemical effects; direct enzymatic or rapid signaling shifts)
  • R: 30 min–3 hr (redox signaling and acute stress-response signaling)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
hepatoP, L,hepatoprotective: Click to Expand ⟱
Source:
Type:
Hepatoprotective is the ability of a chemical substance to prevent damage to the liver.

Grapefruit:
-hepatoprotective potential has emerged from the study of naringenin and naringin.
Blueberries/cranberries:
-proanthocyanidins
Grape:
Nopal (Cactus pear) and tuna (Cactus pear fruit) “Opuntia ficus-indica”:
Chamomile (Matricaria chamomilla or Chamomilla recutita):
Silymarin (Silybum marianum):
Blue green algae spirulina :
Propolis (bee glue):

POLYSACCHARIDES
β-glucans
Scientific Papers found: Click to Expand⟱
2605- Ba,  BA,    Potential therapeutic effects of baicalin and baicalein
- Review, Var, NA - Review, Stroke, NA - Review, IBD, NA - Review, Arthritis, NA - Review, AD, NA - Review, Park, NA
cardioP↑, cardioprotective activities.
Inflam↓, Decreasing the accumulation of inflammatory mediators and improving cognitive function
cognitive↑,
*hepatoP↑, Decreasing inflammation, reducing oxidative stress, regulating the metabolism of lipids, and decreasing fibrosis, apoptosis, and steatosis are their main hepatoprotective mechanisms
*ROS?, Reducing oxidative stress and protecting the mitochondria to inhibit apoptosis are proposed as hepatoprotective mechanisms of baicalin in NAFLD
*SOD↑, Baicalin could reduce the levels of ROS and fatty acid-induced MDA, and increase superoxide dismutase (SOD) and glutathione amounts compared to the control.
*GSH↑,
*MMP↑, Moreover, baicalin could partially restore mitochondrial morphology and increase ATP5A expression and mitochondrial membrane potential (Gao et al., 2022).
*GutMicro↑, After baicalein treatment, a remodelling in the overall structure of the gut microbiota was observed
ChemoSen↑, Besides, a combination of baicalin and doxorubicin could elevate the chemosensitivity of MCF-7 and MDA-MB-231 breast cancer cells
*TNF-α↓, Baicalin can protect cardiomyocytes from hypoxia/reoxygenation injury by elevating the SOD activity and anti-inflammatory responses through reducing TNF-α, enhancing IL-10 levels, decreasing IL-6, and inhibiting the translocation of NF-κB to the nucl
*IL10↑,
*IL6↓,
*eff↑, Studies show that baicalin and baicalein may be effective against IBD by suppressing oxidative stress and inflammation, and regulating the immune system.
*ROS↓,
*COX2↓, baicalein can improve the symptoms of ulcerative colitis by lowering the expression of pregnane X receptor (PXR), (iNOS), (COX-2), and caudal-type homeobox 2 (Cdx2), as well as the NF-κβ and STAT3
*NF-kB↓,
*STAT3↓,
*PGE2↓, Administration of baicalin (30-90 mg/kg) could decrease the levels of prostaglandin E2 (PEG2), myeloperoxidase (MPO), IL-1β, TNF-α, and the apoptosis-related genes including Bcl-2 and caspase-9
*MPO↓,
*IL1β↓,
*MMP2↓, Rheumatoid arthritis RA mouse model by supressing relevant proinflammatory cytokines such as IL-1b, IL-6, MMP-2, MMP-9, TNF-α, iNOS, and COX-2)
*MMP9↓,
*β-Amyloid↓, Alzheimer’s disease (AD) : reduce β-amyloid and trigger non-amyloidogenic amyloid precursor proteins.
*neuroP↑, For instance, administration of baicalin orally for 14 days (100 mg/kg body weight) exhibited neuroprotective effects on pathological changes and behavioral deficits of Aβ 1–42 protein-induced AD in vivo.
*Dose↝, administration of baicalin (500 mg/day, orally for 12 weeks) could improve the levels of total cholesterol, TGs, LDLC and apolipoproteins (APOs), and high-sensitivity C-reactive protein (hs-CRP) in patients with rheumatoid arthritis and coronary arte
*BioAv↝, the total absorption of baicalin depends on the activity of intestinal bacteria to convert baicalin to baicalein as the first step.
*BioAv↝, Kidneys, liver, and lungs are the main organs in which baicalin accumulates the most.
*BBB↑, Baicalin and baicalein can pass through the blood brain barrier (BBB)
*BDNF↑, mechanism of action for baicalein is illustrated in Figure 3. Activation of the BDNF/TrkB/CREB pathway, inhibition of NLRP3/Caspase-1/GSDMD pathway,

2614- Ba,    Therapeutic potentials of baicalin and its aglycone, baicalein against inflammatory disorders
- Review, NA, NA
*toxicity↓, These flavonoids have almost no toxicity to human normal epithelial, peripheral and myeloid cells
*antiOx↑, antioxidant and anti-inflammatory activities are largely due to their abilities to scavenge the reactive oxygen species (ROS)
*Inflam↓,
*ROS↓,
*NF-kB↓, by attenuating the activity of NF-κB and suppressing the expression of several inflammatory cytokines and chemokines including monocyte chemotactic protein-1 (MCP-1)
*MCP1↓,
*hepatoP↑, Both baicalin and baicalein ... including antioxidant, anti-inflammatory, anticancer, anticardiovascular, antidiabetic, hepatoprotective, antiviral, anti-ulcerative colitis, antithrombotic, eye protective and neuroprotective activities
*neuroP↑,

2613- Ba,    Hepatoprotective Effect of Baicalein Against Acetaminophen-Induced Acute Liver Injury in Mice
- in-vivo, Nor, NA
*hepatoP↑, baicalein significantly ameliorated APAP-exposed liver damage and histological hepatocyte changes
*MDA↓, baicalein (50 or 100 mg/kg) pretreatment significantly inhibited liver MDA level (p < 0.05; Figure 4), increased SOD, CAT and GSH activity.
*SOD↑,
*Catalase↑,
*GSH↑,
*MAPK↓, Baicalein Prevented the MAPK Pathway Activation
*p‑JAK2↓, BAI Suppressed the Expression of p-JAK2 and p-STAT3 Proteins in APAP Liver Injury
*p‑STAT3↓,
*ALAT↓, our experimental results suggested that serum ALT and AST levels were obviously alleviated by Baicalein in a dose-dependent manner
*AST↓,
*ROS↓, hepatoprotective role of BAI via attenuating oxidative stress
*antiOx↑, hepatoprotective activity of Baicalein might be associated with its antioxidative capacity.

2610- Ba,    Hepatoprotective effects of baicalein against CCl4-induced acute liver injury in mice
- in-vivo, Nor, NA
*TNF-α↑, elevated the serum level of TNF-α and IL-6 at the early phase, which indicated that baicalein could facilitate the initiating events in liver regeneration.
*IL6↑,
*hepatoP↑,

2609- Ba,    Baicalein: unveiling the multifaceted marvel of hepatoprotection and beyond
- Review, NA, NA
*hepatoP↑, baicalein's hepatoprotective action against different toxicity models (acetaminophen, cisplatin, doxorubicin, CCL4, monocrotaline, & d-galactosamine).
*neuroP↑, key pharmacological activities of baicalein against neurotoxicity (6-OHDA, rotenone, d-galactose, stroke, alzheimer, & sclerosis),
*Inflam↓, inflammation (arthritis, pulmonary fibrosis, & LPS-induced sepsis

2607- Ba,  SIL,    Baicalein Enhances the Oral Bioavailability and Hepatoprotective Effects of Silybin Through the Inhibition of Efflux Transporters BCRP and MRP2
- in-vivo, Nor, NA
*BioEnh↑, baicalein significantly increased the area under the curve (AUC) and Cmax of silybin and its conjugates, suggesting enhanced absorption in vivo.
*hepatoP↑, Moreover, coadministration of silybin with baicalein boosted the liver protective, antioxidant, and anti-inflammatory effects of silybin
*antiOx↑,
*Inflam↓,

5248- Ba,  BA,  doxoR,    Baicalin and Baicalein Enhance Cytotoxicity, Proapoptotic Activity, and Genotoxicity of Doxorubicin and Docetaxel in MCF-7 Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, Nor, HUVECs
toxicity↝, We have found that baicalin and baicalein demonstrated cytotoxicity towards both cell lines, with more potent effects observed in baicalein.
ChemoSen↑, Both flavonoids, baicalin (167 µmol/L) and baicalein (95 µmol/L), synergistically enhanced the cytotoxic, proapoptotic, and genotoxic activity of doxorubicin and docetaxel in breast cancer cells.
selectivity↑, Surprisingly, low concentrations of baicalin and baicalein had a greater effect on MCF-7 viability. A
Apoptosis↑, Induction of Apoptosis and Necrosis by Baicalin and Baicalein Used alone and in Combination with Anticancer Drugs
necrosis↑,
MMP↓, After treatment with baicalin and baicalein at high concentrations (IC50), the ΔΨm of cancer cells was diminished to 30% of the control value
DNAdam↑, DNA Damage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
cl‑PARP↑, PARP Cleavage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
MRP1↓, Moreover, baicalin and baicalein reduced cisplatin resistance by inhibiting the expression of genes involved in drug resistance, such as MRP1 [30] and Bcl-2, and via the Akt/mTOR and Nrf2/Keap 1 pathway [26].
Bcl-2↓,
hepatoP↑, baicalin and baicalein can also help decrease the side effects of cisplatin treatment by protecting the liver from damage [31]
cardioP↑, Similar to baicalein, baicalin also significantly protects against doxorubicin’s cardiotoxicity.
BioAv↝, This is because baicalein has a smaller size and high lipophilicity, contributing to fast absorption and an improved ability to penetrate cells [60].

2626- Ba,    Molecular targets and therapeutic potential of baicalein: a review
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
AntiCan↓, anticancer, antidiabetic, antimicrobial, antiaging, neuroprotective, cardioprotective, respiratory protective, gastroprotective, hepatic protective, and renal protective effects
*neuroP↑,
*cardioP↑, Cardioprotective action of baicalein
*hepatoP↑,
*RenoP↑, baicalein’s capacity to lessen cisplatin-induced nephrotoxicity is probably due, at least in part, to the attenuation of renal oxidative and/or nitrative stress
TumCCA↑, Baicalein induces G1/S arrest in lung squamous carcinoma (CH27) cells by downregulating CDK4 and cyclin D1, as well as upregulating cyclin E
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↑,
BAX↑, SGC-7901 cells showed that when baicalein was administered, Bcl-2 was downregulated and Bax was increased
Bcl-2↓,
VEGF↓, Baicalein inhibits the synthesis of vascular endothelial growth factor (VEGF), HIF-1, c-Myc, and nuclear factor kappa B (NF-κB) in the G1 and S phases of ovarian cancer cell
Hif1a↓,
cMyc↓,
NF-kB↓,
ROS↑, Baicalein produced intracellular reactive oxygen species (ROS) and activated BNIP3 to slow down the development and hasten the apoptosis of MG-63,OS cell
BNIP3↑,
*neuroP↑, Baicalein exhibits neuroprotective qualities against amyloid (AN) functions by preventing AN from aggregating in PC12 neuronal cells to cause A𝛽-induced cytotoxicity
*cognitive↑, baicalein encourages non-amyloidogenic processing of APP, which lowers the generation of A𝛽 and enhances cognitive function
*NO↓, baicalein effectively reduced NO generation and iNOS gene expression
*iNOS↓,
*COX2↓, Baicalein therapy significantly decreased the expression of COX-2 and iNOS, as well as PGE2 and NF-κB, indicating a protective effect against cerebral I/R injury.
*PGE2↓,
*NRF2↑, Baicalein therapy markedly elevated nuclear Nrf2 expression and AMPK phosphorylation in the ischemic cerebral cortex
*p‑AMPK↑,
*Ferroptosis↓, Baicalein suppressed ferroptosis associated with 12/15-LOX, hence lessening the severity of post-traumatic epileptic episodes generated by FeCl3
*lipid-P↓, HT22 cells were damaged by ferroptosis, which is mitigated by baicalein may be due to its lipid peroxidation inhibitor
*ALAT↓, Baicalin lowers the raised levels of hepatic markers alanine transaminase (ALT), aspartate aminotransferase (AST)
*AST↓,
*Fas↓, Baicalin has also been shown to suppress apoptosis, decrease FAS protein expression, block the caspase-8 pathway, and decrease Bax protein production
*BAX↓,
*Apoptosis↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 2,   necrosis↑, 1,  

Autophagy & Lysosomes ⓘ

BNIP3↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↑, 1,   TumCCA↑, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   ChemoSen↑, 2,   MRP1↓, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiCan↓, 1,   cardioP↑, 2,   cognitive↑, 1,   hepatoP↑, 1,   toxicity↝, 1,  
Total Targets: 27

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 1,   Ferroptosis↓, 1,   GSH↑, 2,   lipid-P↓, 1,   MDA↓, 1,   MPO↓, 1,   NRF2↑, 1,   ROS?, 1,   ROS↓, 3,   SOD↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2,   p‑AMPK↑, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   BAX↓, 1,   Fas↓, 1,   Ferroptosis↓, 1,   iNOS↓, 1,   MAPK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,   p‑STAT3↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL10↑, 1,   IL1β↓, 1,   IL6↓, 1,   IL6↑, 1,   Inflam↓, 3,   p‑JAK2↓, 1,   MCP1↓, 1,   NF-kB↓, 2,   PGE2↓, 2,   TNF-α↓, 1,   TNF-α↑, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,  

Protein Aggregation ⓘ

β-Amyloid↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 2,   BioEnh↑, 1,   Dose↝, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 2,   AST↓, 2,   GutMicro↑, 1,   IL6↓, 1,   IL6↑, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 1,   hepatoP↑, 7,   neuroP↑, 5,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 55

Scientific Paper Hit Count for: hepatoP, L,hepatoprotective
8 Baicalein
2 Baicalin
1 Silymarin (Milk Thistle) silibinin
1 doxorubicin
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:38  Target#:1179  State#:%  Dir#:%
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