Baicalein / neuroP Cancer Research Results

Ba, Baicalein: Click to Expand ⟱
Features:

Baicalein — Baicalein is a polyphenolic flavone aglycone found primarily in Scutellaria baicalensis and related botanicals, and is the active unconjugated counterpart of baicalin after intestinal/microbial deconjugation and re-conjugation cycling. It is formally classified as a small-molecule natural-product flavonoid with pleiotropic signaling, redox, metabolic, and enzyme-modulatory activity. Standard abbreviations include Ba or BE. In cancer literature it is best characterized as a multi-target preclinical anticancer scaffold rather than an established oncology drug, with relatively strong mechanistic support for apoptosis induction, survival-pathway suppression, anti-invasive signaling, and 12-lipoxygenase inhibition, but with major translational constraints from poor aqueous solubility, extensive first-pass glucuronidation/sulfation, transporter-enzyme interactions, and the likelihood that many in-vitro exposure levels exceed typical systemic aglycone exposure.

Primary mechanisms (ranked):

  1. 12-lipoxygenase inhibition with downstream suppression of pro-survival, pro-migratory, and pro-angiogenic lipid signaling.
  2. Intrinsic apoptosis induction via mitochondrial destabilization, cytochrome-c release, caspase-9/3 activation, and BAX:BCL-2 shift.
  3. PI3K/AKT survival-axis repression, often with PTEN restoration and reduced downstream anti-apoptotic signaling.
  4. Redox stress modulation with tumor-context ROS↑ and impaired antioxidant buffering, but normal-cell antioxidant protection in oxidative-injury models.
  5. ER-stress and Ca²⁺ stress coupling that amplifies mitochondrial commitment to cell death.
  6. Suppression of glycolysis / hypoxia adaptation, including HIF-1α, HK2, LDHA, PDK1, PKM2, and GLUT1 in relevant models.
  7. Anti-invasive / anti-metastatic signaling through MMP2/MMP9 and related migration programs.
  8. Anti-angiogenic signaling with VEGF reduction.
  9. Contextual chemo- and radiosensitization in selected models.

Bioavailability / PK relevance: Oral translation is constrained by very low water solubility and extensive intestinal/hepatic phase-II metabolism to glucuronide and sulfate conjugates. Human phase-I data show rapid absorption of tablet formulations with peak plasma levels around 2 hours, steady state after repeated dosing, and major circulating/excreted metabolite burden rather than sustained high parent-aglycone exposure. Microbiota, UGT-dependent reconjugation, and transporter/CYP interactions are clinically relevant variables. Intestinal microbiota are mechanistically relevant because baicalin is converted to baicalein before absorption. Poor translational PK is reinforced by very low aqueous solubility, reported around 16.82 μg/mL, and by formulation studies showing large exposure gains after cocrystal/nanodelivery approaches.

In-vitro vs systemic exposure relevance: Many anticancer cell studies use roughly 10–50 μM and sometimes higher. That generally exceeds typical reported average human plasma exposure for parent baicalein after oral dosing, so direct translation of higher-concentration in-vitro effects should be treated cautiously unless formulation enhancement, local delivery, tissue enrichment, conjugate deconjugation, or combination use is specifically justified.

Clinical evidence status: Strong preclinical evidence across multiple tumor models; limited animal efficacy support; human clinical experience is mainly phase-I safety/PK and non-oncology development contexts. There is no established cancer indication or mainstream regulatory oncology deployment as of March 12, 2026.

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).

Mechanistic table

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 12-Lipoxygenase axis ↓ 12-LOX, ↓ 12-HETE-linked survival / migration signaling ↔ or modest effect P, R Direct target-level antitumor leverage One of the more mechanistically specific baicalein actions. Supports anti-proliferative, anti-migratory, and anti-angiogenic behavior in susceptible tumors.
2 Mitochondria / MPTP ↓ ΔΨm, ↑ mitochondrial dysfunction, ↑ Cyt-c release ↔ or protected in oxidative-injury models R, G Intrinsic apoptosis commitment Mitochondrial collapse is a major convergence point downstream of redox, ER-stress, and survival-pathway suppression.
3 Caspase apoptosis program ↑ BAX, ↓ Bcl-2, ↑ Casp9, ↑ Casp3, ↑ apoptosis ↔ minimal activation G Cell-death execution Widely reported across tumor models; often follows mitochondrial injury rather than representing the earliest event.
4 PI3K / AKT / PTEN axis ↓ PI3K, ↓ p-AKT, ↑ PTEN ↔ or context-dependent R, G Survival suppression A central non-redox pathway that helps explain apoptosis sensitization, cell-cycle arrest, and metabolic downshift.
5 ROS balance ↑ ROS (dose-dependent) or ROS⇅ depending on model ↓ ROS under oxidative challenge P, R, G Tumor-selective redox stress Dual behavior is important: pro-oxidant pressure is common in malignant cells, whereas antioxidant cytoprotection is well documented in stressed non-malignant cells.
6 NRF2 / HO-1 / GSH antioxidant buffering ↓ NRF2, ↓ HO-1, ↓ GSH (context-dependent) ↑ NRF2, ↑ HO-1, ↑ GSH, ↑ SOD / catalase R, G Selectivity gate This divergent redox-buffer response likely contributes to cancer-versus-normal selectivity, but it is model-dependent and should not be overstated as universal.
7 ER stress and Ca²⁺ stress coupling ↑ ER stress, ↑ CHOP, ↑ UPR, ↑ Ca²⁺ dysregulation ↔ buffered homeostasis R, G Stress amplification Likely helps transmit redox/survival perturbation into irreversible mitochondrial death signaling.
8 Glycolysis / HIF-1α adaptation ↓ HIF-1α, ↓ HK2, ↓ LDHA, ↓ PDK1, ↓ PKM2, ↓ GLUT1, ↓ glycolysis ↔ G Metabolic constraint Most convincing in hypoxia-adaptation and gastric / radioresistance models. Usually reflects later transcriptional or adaptation-level effects.
9 NF-κB and MAPK / ERK signaling ↓ NF-κB, MAPK / ERK modulation (often ↓ ERK tone) ↔ or context-dependent P, R, G Signal reprogramming Supports lower inflammatory-survival tone, apoptosis sensitization, and reduced proliferation, but exact direction within MAPK branches can vary by tumor model.
10 Invasion / metastasis axis ↓ MMP2, ↓ MMP9, ↓ migration / invasion ↔ G Anti-invasive phenotype Phenotypically important and relatively consistent, though usually secondary to broader signaling reprogramming.
11 Angiogenesis axis ↓ VEGF, ↓ microvessel support ↔ G Anti-angiogenic support Supported by xenograft and lung-cancer data; best viewed as an adjunct downstream effect rather than sole primary mechanism.
12 Radiosensitization / chemosensitization ↑ treatment sensitivity (context-dependent) Potential normal-tissue protection in oxidative-injury contexts G Combination-use leverage Mechanistically plausible via HIF-1α/glycolysis suppression, NF-κB restraint, and apoptosis priming, but still preclinical and heterogeneous.
13 Clinical Translation Constraint Low parent exposure, variable microbiota handling, rapid conjugation, likely concentration gap May favor safety but complicates efficacy extrapolation G Delivery limitation Poor solubility, strong first-pass metabolism, conjugate predominance, possible CYP/transporter interactions, and lack of oncology-grade clinical validation are the main barriers.

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)
neuroP, neuroprotective: Click to Expand ⟱
Source:
Type:
Neuroprotective refers to the ability of a substance, intervention, or strategy to preserve the structure and function of nerve cells (neurons) against injury or degeneration.
-While cancer and neurodegenerative processes might seem distinct, there is significant overlap in terms of treatment-related neurotoxicity, shared molecular mechanisms, and the potential for therapies that provide neuroprotection during cancer treatment.
Scientific Papers found: Click to Expand⟱
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↑,

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↓,

2623- Ba,    Activation of the Nrf2/HO-1 signaling pathway contributes to the protective effects of baicalein against oxidative stress-induced DNA damage and apoptosis in HEI193 Schwann cells
- in-vitro, Nor, HEI193
*DNAdam↓, Our results showed that baicalein effectively inhibited H2O2-induced cytotoxicity and DNA damage associated with the inhibition of reactive oxygen species (ROS) accumulation.
*ROS↓,
*Bax:Bcl2↓, increased the Bax/Bcl-2 ratio
*p‑NRF2↑, baicalein increased not only the expression but also the phosphorylation of nuclear factor-erythroid 2 related factor 2 (Nrf2) and promoted the expression of heme oxygenase-1 (HO-1)
*HO-1↑, it is well known that the antioxidant efficacy of baicalein is related to the activation of the Nrf2/HO-1 signaling pathway
*neuroP↑, suggested that baicalein may have a beneficial effect on the prevention and treatment of peripheral neuropathy induced by oxidative stress.
*MMP↑, inhibitory effect of baicalein on MMP reduction

2611- Ba,    Baicalein as a potent neuroprotective agent: A review
- Review, Nor, NA - Review, AD, NA - Review, Park, NA
*neuroP↑, A number of studies have reported that baicalein has potent neuroprotective properties under in vitro as well as in vivo systems
*ROS↓, Baicalein effectively prevents Alzheimer's and Parkinson's diseases by reducing oxidative stress, inhibiting aggregation of disease-specific amyloid proteins,
*β-Amyloid↓,

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

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,

5508- Ba,    Neuroprotective effects of baicalin and baicalein on the central nervous system and the underlying mechanisms
- Review, Stroke, NA - Review, Park, NA - Review, AD, NA
*neuroP↑, Recent studies have shown its good protective effect on neurons and brain tissues [14].
*antiOx↑, strong anti-inflammatory and antioxidant properties.
*Inflam↓,
*BioAv↝, When taken orally, baicalin is converted to baicalein via β-glucuronidase (GUS), which is produced by the intestinal flora.
*BioAv↑, Pharmacokinetics indicate that baicalein has a higher absorption rate than baicalein [19], but once it is absorbed, baicalein is quickly degraded in the bloodstream, yielding baicalein
*Half-Life↝, The distribution half-life and elimination half-life of baicalin in the CSF of normal rats are 0.8868 and 26.0968 min, respectively.
*TLR4↓, Inhibition of the TLR4/MyD88/NF-κB signal
*NF-kB↓,
*iNOS↓, decreasing the synthesis of iNOS, COX2, and TNF-α
*COX2↓,
*TNF-α↓,
*12LOX↓, downregulation of 12/15-LOX after cerebral ischemia
*NLRP3↓, Inhibition of the expression of NLRP3, HT-22 cells
*ROS↓, Decrease in the ROS levels in the ICH, thus inhibiting high NLRP3
*IL1β↓, Reduced the amounts of IL-1β and IL-6 and inhibited the activation of the NLRP3 inflammasome
*IL6↓,
*GSK‐3β↓, Inhibiting the activation of the GSK3β/NF-κB/NLRP3 signaling pathway
*NRF2↑, Fang et al. reported that the activation of the Akt pathway resulted in increased Nrf2 nuclear translocation and immunoreactivity in a group treated with baicalin
*BBB↑, baicalein effectively crosses the blood‒brain barrier (BBB) and stimulates the Nrf2/HO-1 pathway via specialized brain-targeted exosomes
*SOD↑, increased serum levels of SOD and GSH-Px.
*GPx↑,
*MDA↓, baicalin inhibited the ROS production and reduced MDA levels in brain tissues from a rat model of cerebral I/R injury induced by middle cerebral artery occlusion (MCAO).

5502- Ba,    An overview of pharmacological activities of baicalin and its aglycone baicalein: New insights into molecular mechanisms and signaling pathways
- Review, Var, NA
*AntiCan↑, antibacterial, antiviral, anticancer, anticonvulsant, anti-oxidant, hepatoprotective, and neuroprotective effects.
*antiOx↑,
*hepatoP↑,
*neuroP↑,
*ROS↓, pharmacological properties of baicalin and baicalein are due to their abilities to scavenge reactive oxygen species (ROS)
Ca+2↑, Baicalein mainly induced apoptosis through Ca+2 influx via Ca2+ release from the reticulum to cytosol dependent on phospholipase C protein
ROS↑, ROS production is associated with baicalein-induced apoptosis via Ca2+-dependent apoptosis in tongue and breast cancer cells (78, 79)
BAX↑, The level of Bax/Bcl-2 increased and caspase-3 and -9 were activated following the release of cytochrome C (80).
Casp3↑,
Casp9↑,
Cyt‑c↑,
MMP↓, In gastric cancer cells, baicalein mediated apoptosis in a dose-dependent manner through disruption of mitochondrial membrane potential
Mcl-1↓, In pancreatic cancer cells, baicalein induced apoptosis via suppression of the Mcl-1 protein.
PI3K↓, In HepG2 cells, baicalin-copper induced apoptosis through down-regulation of phosphoinositide-3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway
Akt↓,
mTOR↓,
BAD↓, Studies demonstrated that baicalein treatment suppressed Bad, ERK1/2 phosphorylation, and MEK1 expression both in vitro and in vivo.
ERK↓,
MEK↓,
DR5↑, Baicalein enhanced the activity of death receptor-5 (DR5) in prostate cancer PC3 cells.
Fas↑, baicalin is the active ingredient that acts as Fas ligand and caused up-regulation of Fas protein (89).
TumMeta↓, Baicalin/baicalein not only induced apoptosis in cancer cells but also suppressed metastasis.
EMT↓, both baicalin and baicalein inhibited epithelial-mesenchymal transition (EMT) through the suppression of TGF-β in breast epithelial cells through the NF-κB pathway (92).
SMAD4↓, baicalein suppressed metastasis in gastric cancer through inactivation of the Smad4/TGF-β pathway (93).
TGF-β↓,
MMP9↓, baicalin and baicalein inhibition of the expression level of matrix metalloproteinases (MMP) such as MMP-9 and MMP-2 in liver, breast, lung, ovarian, gastric, and colorectal cancers and glioma
MMP2↓,
HIF-1↓, Baicalin attenuated lung metastasis through inhibition of hypoxia-inducible factor (HIF)
12LOX↓, Baicalein acts as an anticancer agent via inhibiting 12-lipooxygenase (12-LOX),

4305- Ba,    Study on the Molecular Mechanism of Baicalin Phosphorylation of Tau Protein Content in a Cell Model of Intervention Cognitive Impairment
- in-vitro, NA, SH-SY5Y
*cognitive↑, In cell experiments, baicalein presented a positive impact on mild cognitive impairment by elevating P-AKT1 and P-GSK-3β levels while reducing the overall amount of P-tau.
*p‑Akt↑,
*p‑GSK‐3β↑,
*p‑tau↓,
*neuroP↑, baicalein demonstrates a neuroprotective by modulating pathways such as the NF-κB/MAPK signaling pathway and the AMPK/Nrf2 pathway.
*NF-kB↓,
*AMPK↑,
*NRF2↑,

2483- Ba,    Baicalein and 12/15-Lipoxygenase in the Ischemic Brain
- in-vivo, Stroke, NA
*12LOX↓, The natural product baicalein is a specific inhibitor of 12/15-lipoxygenase, but it also has antioxidant properties.
*antiOx↓,
*neuroP↑, in vivo data suggest that 12/15-lipoxygenase contributes to brain damage after stroke, and that 12/15-LOX inhibition by baicalein is neuroprotective.

2482- Ba,    Modulation of Neuroinflammation in Poststroke Rehabilitation: The Role of 12/15-Lipoxygenase Inhibition and Baicalein
- Review, Stroke, NA
*12LOX↓, Baicalein, a potent 12/15-LOX (12/15-lipoxygenase) inhibitor
*neuroP↑, demonstrates neuroprotective effects by reducing inflammatory lipid mediators, modulating key inflammatory pathways, and attenuating oxidative stress.
*eff↑, Experimental studies indicate that baicalein can diminish infarct size and neurological deficits while improving safety and tolerability


Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MEK↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,   cMyc↓, 1,  

Cell Death ⓘ

Akt↓, 1,   BAD↓, 1,   BAX↑, 2,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   DR5↑, 1,   Fas↑, 1,   Mcl-1↓, 1,  

Autophagy & Lysosomes ⓘ

BNIP3↑, 1,  

Cell Cycle & Senescence ⓘ

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

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 1,   mTOR↓, 1,   PI3K↓, 1,  

Migration ⓘ

Ca+2↑, 1,   MMP2↓, 1,   MMP9↓, 1,   SMAD4↓, 1,   TGF-β↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

HIF-1↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,  

Functional Outcomes ⓘ

AntiCan↓, 1,   cardioP↑, 1,   cognitive↑, 1,  
Total Targets: 39

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 3,   Ferroptosis↓, 1,   GPx↑, 1,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   MPO↓, 1,   NRF2↑, 3,   p‑NRF2↑, 1,   ROS?, 1,   ROS↓, 6,   SOD↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 2,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 3,   ALAT↓, 1,   AMPK↑, 1,   p‑AMPK↑, 1,  

Cell Death ⓘ

p‑Akt↑, 1,   Apoptosis↓, 1,   BAX↓, 1,   Bax:Bcl2↓, 1,   Fas↓, 1,   Ferroptosis↓, 1,   iNOS↓, 2,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,   p‑GSK‐3β↑, 1,   STAT3↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 1,  

Barriers & Transport ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   IL10↑, 1,   IL1β↓, 2,   IL6↓, 2,   Inflam↓, 3,   MCP1↓, 1,   NF-kB↓, 4,   PGE2↓, 2,   TLR4↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,   p‑tau↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,   β-Amyloid↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 3,   Dose↝, 1,   eff↑, 2,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

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

Functional Outcomes ⓘ

AntiCan↑, 1,   cardioP↑, 1,   cognitive↑, 2,   hepatoP↑, 5,   neuroP↑, 12,   RenoP↑, 1,   toxicity↓, 1,  
Total Targets: 64

Scientific Paper Hit Count for: neuroP, neuroprotective
11 Baicalein
1 Baicalin
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#:1105  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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