Narrow Results

Much progress has been made in the pharmacology of Traditional Chinese Medicine (TCM). However, the question on how to investigate pharmacokinetics of TCM extract remains. In this study, we selected a new TCM extract YL2000 developed in our laboratory as the research object and investigated both the pharmacokinetics of baicalin and berberine in YL2000 and the pharmacodynamics of YL2000 in febrile rats. The correlation analysis between the time-concentration curves of baicalin and berberine and the time-effect curve of YL2000 was conducted in plasma by statistical methods. The results showed that the time-effect data of anti-pyretic effect of YL2000 had a negative correlation (r=-0.8312, P<0.1) with the time-concentration data of baicalin in plasma, but had no correlation (r=0.01368, P>0.5) with berberine. These data suggested that baicalin could be selected as a marker of anti-pyretic effect, and that YL2000 could be used to treat fevers according to the disposition of baicalin in vivo.

In this study, we also proposed that one or more active elements in TCM extracts could be selected to represent the pharmacokinetics of TCM extracts in vivo, combined with the pharmacodynamics of TCM extract.

Acute lymphoblastic leukemia (ALL), especially T-acute lymphoblastic leukemia (T-ALL), is a common childhood malignant neoplastic disorder. Chemotherapy agents, particularly those that can induce apoptosis, are the major intervening strategy in the treatment of ALL. In this study, we investigated in T-ALL cell line, CCRF-CEM, the in vitro cytotoxic effect and the mechanism of action of baicalin, a compound extracted from Scutellaria baicalensis Georgi and S. rivularis Benth (Labiateae). Results demonstrated that baicalin displayed a remarkable cytotoxic effect in CCRF-CEM, with an IC₅₀ value of 10.6 μg/ml. It triggered apoptotic effect by fragmentizing cellular DNA and arrested the cell cycle at G₀/G₁ phase. Baicalin (37.5 μg/ml)had not effected the expression of p53 and Fas protein. It was shown to decline the expression of Bcl-2 (22.0 pg/ml), which consequently caused the loss (52.7%)of transmembrane potential (ΔΨm) in the mitochondria after 72 hours of treatment. Baicalin (37.5 μg/ml) also elevated the amount of cytosolic cytochrome c (19.2 μg/ml), which finally triggered the activation of caspase-3 (50.1 pmol/min). In conclusion, baicalin was found to induce apoptosis in T-ALL cell lines through multiple pathways. This finding encourages further investigation of baicalin in its role as a potential candidate for chemotherapeutic agents in T-ALL.

Baicalin is a flavonoid present in many traditional Chinese medicines. A number of studies show that baicalin has anti-inflammatory actions and protects against a variety of tissue and organ injuries. The effect of baicalin in lipopolysaccharide (LPS)-induced acute lung injury is not well studied. In this study, typically acute lung injury was induced in rat by intratracheal injection of LPS, which increased lactate dehydrogenase activity and protein content in bronchoalveolar lavage fluid, wet/dry lung weight ratio, Evan's blue dye leakage, and neutrophil infiltration. Baicalin (20 mg/kg) was administrated 1 hour before or 30 min after LPS injection. Both pre and post-treatment with baicalin attenuated the increase of these parameters and improved histological finding. Our results suggest that baicalin has a therapeutic effect on LPS-induced acute lung injury.

Baicalin, one kind of Chinese herbal medicine with anti-inflammatory and anti-oxidant property, has been commonly used as a clinical medicine. However, little has been known about the effects of Baicalin on ultraviolet (UV) induced photo-aging and photo-carcinogenesis. The photoproduct is critical to the initial event of UV-induced photo-carcinogenesis. The purpose of the present study was to investigate whether Baicalin, in immortalized human keratinocyte HaCaT cells, could inhibit ultraviolet-B (UVB) induced skin damage and its possible underlying mechanisms, such as inhibiting UVB-induced cytotoxicity and apoptosis, cyclobutane pyrimidine dimers (CPDs), down-regulating the expression of regulatory proteins which are related to cell apoptosis and DNA damage/repair. Our study revealed that Baicalin treatment could inhibit the UVB-induced cytotoxicity, apoptosis and CPD level. It also decreased the mRNA expression of apoptosis-regulatory genes (p53-p21 and c-fos), the protein levels of p53, proliferating cell nuclear antigen (PCNA) and repair protein A (RPA), and the secretion of cytokines [interleukin(IL)-6 and tumor necrosis factor (TNF-α)]. These results suggested that Baicalin may have an inhibitory effect on the UVB-induced photo-damage by blocking the relevant cytokine secretion and expression of p53-p21, c-fos, PCNA and RPA genes.

The Chinese herbal medicine Huang Qin (Radix Scutellariae) had been used for restless fetus for hundreds of years in China, however, little attention had been given to the components of the herb, specifically its ability to exert abortion-preventing effects at the maternal fatal interface. The present study was carried out to investigate the protective effects of baicalin and the possible mechanisms on pregnancies. Baicalin (at 10, 20, and 50 mg/kg BW respectively) was gavaged to bromocriptine-treated mice from gestation day (GD) 1 through GD 7. Abortion rates were calculated and the changes of interferon-γ (IFN-γ), interleukin-10 (IL-10) and progesterone were assayed on different gestation days. Results showed that the embryonic death rates were significantly decreased in groups supplemented with 20 or 50 mg/kg BW of baicalin, accompanied with reduced IFN-γ and enhanced progesterone contents. Moreover, the highest levels of IFN-γ appeared on GD 5 both in the control and in baicalin treated groups. It is concluded that baicalin can exert an anti-abortive effect by cutting down the production of IFN-γ and elevating the levels of progesterone in a dose dependent manner and IFN-γ is involved in an inflammatory reaction which is beneficial for a successful implantation.

Ultraviolet A (UVA) radiation contributes to skin photoaging. Baicalin, a plant-derived flavonoid, effectively absorbs UV rays and has been shown to have anti-oxidant and anti-inflammatory properties that may delay the photoaging process. In the current study, cultured human skin fibroblasts were incubated with 50 μg/ml baicalin 24 hours prior to 10 J/cm² UVA irradiation. In order to examine the efficacy of baicalin treatment in delaying UVA-induced photoaging, we investigated aging-related markers, cell cycle changes, anti-oxidant activity, telomere length, and DNA damage markers. UVA radiation caused an increased proportion of β-Gal positive cells and reduced telomere length in human skin fibroblasts. In addition, UVA radiation inhibited TGF-β1 secretion, induced G1 phase arrest, reduced SOD and GSH-Px levels, increased MDA levels, enhanced the expression of MMP-1, TIMP-1, p66, p53, and p16 mRNA, reduced c-myc mRNA expression, elevated p53 and p16 protein expression, and reduced c-myc protein expression. Baicalin treatment effectively protected human fibroblasts from these UVA radiation-induced aging responses, suggesting that the underlying mechanism involves the inhibition of oxidative damage and regulation of the expression of senescence-related genes, including those encoding for p53, p66^Shc and p16.

Sho-saiko-to is an herbal medicine that is known to have diverse pharmacological activities and has been used for the treatment of various infectious diseases. Here, we examined the effects of baicalin, a compound isolated from Sho-saiko-to, and the effects of the iron chelator quinolinic acid on the Fenton reaction. The control reaction mixture contained 0.1 M 5,5-dimethyl-1-pyrroline N-oxide (DMPO), 0.2 mM H₂O₂, 0.2 mM FeSO₄(NH₄)₂SO₄, and 40 mM sodium phosphate buffer (pH 7.4). Upon the addition of 0.6 mM baicalin or quinolinic acid to the control reaction mixture, the ESR peak heights of DMPO/OH radical adducts were measured as 32% ± 1% (baicalin) and 166% ± 27% (quinolinic acid) of that of the control mixture. In order to clarify why baicalin and quinolinic acid exerted opposite effects on the formation of hydroxyl radicals, we measured oxygen consumption in the presence of either compound. Upon the addition of 0.6 mM baicalin (or quinolinic acid) to the control reaction mixture without DMPO and H₂O₂, the relative oxygen consumption rates were found to be 449% ± 40% (baicalin) and 18% ± 9% (quinolinic acid) of that of the control mixture without DMPO and H₂O₂, indicating that baicalin facilitated the transfer of electrons from Fe²⁺ to dissolved oxygen. Thus, the great majority of Fe²⁺ turned into Fe³⁺, and the formation of hydroxyl radicals was subsequently inhibited in this reaction.

The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) receives nociceptive afferent inputs from thin-myelinated A$\delta$ fibers and unmyelinated C fibers and has been shown to be involved in the processing of orofacial nociceptive information. Scutellaria baicalensis Georgi (Huang-Qin, SbG), one of the 50 fundamental herbs of Chinese herbology, has been used historically as anti-inflammatory and antineoplastic medicine. Baicalin, one of the major compounds of SbG, has been reported to have neuroprotective, anti-inflammatory and analgesic effects. However, the receptor type activated by baicalin and its precise action mechanism on the SG neurons of Vc have not yet been studied. The whole-cell patch clamp technique was performed to examine the ion channels activated by baicalin on the SG neurons of Vc. In high Cl${}^{-}$ pipette solution, the baicalin (300$\mu$M) induced repeatable inward currents ($-24.8\pm 3.57$pA, $n=19$) without desensitization on all the SG neurons tested. Further, the inward currents showed a concentration (0.1–3mM) dependent pattern. The inward current was sustained in the presence of tetrodotoxin (0.5$\mu$M), a voltage sensitive Na${}^{+}$ channel blocker. In addition, baicalin-induced inward currents were reduced in the presence of picrotoxin (50$\mu$M), a GABA_A receptor antagonist, flumazenil (100$\mu$M), a benzodiazepine-sensitive GABA_A receptor antagonist, and strychnine (2$\mu$M), a glycine receptor antagonist, respectively. These results indicate that baicalin has inhibitory effects on the SG neurons of the Vc, which are due to the activation of GABA_A and/or the glycine receptor. Our results suggest that baicalin may be a potential target for orofacial pain modulation.

Acetaminophen (APAP) overdose causes hepatocytes necrosis and acute liver failure. Baicalin (BA), a major flavonoid of Scutellariae radix, has potent hepatoprotective properties in traditional medicine. In the present study, we investigated the protective effects of BA on a APAP-induced liver injury in a mouse model. The mice received an intraperitoneal hepatotoxic dose of APAP (300mg/kg) and after 30min, were treated with BA at concentrations of 0, 15, 30, or 60mg/kg. After 16h of treatment, the mice were sacrificed for further analysis. APAP administration significantly elevated the serum alanine transferase (ALT) enzyme levels and hepatic myeloperoxidase (MPO) activity when compared with control animals. Baicalin treatment significantly attenuated the elevation of liver ALT levels, as well as hepatic MPO activity in a dose- dependent manner (15–60mg/kg) in APAP-treated mice. The strongest beneficial effects of BA were seen at a dose of 30mg/kg. BA treatment at 30mg/kg after APAP overdose reduced elevated hepatic cytokine (TNF-$\alpha$ and IL-6) levels, and macrophage recruitment around the area of hepatotoxicity in immunohistochemical staining. Significantly, BA treatment can also decrease hepatic phosphorylated extracellular signal-regulated kinase (ERK) expression, which is induced by APAP overdose. Our data suggests that baicalin treatment can effectively attenuate APAP-induced liver injury by down-regulating the ERK signaling pathway and its downstream effectors of inflammatory responses. These results support that baicalin is a potential hepatoprotective agent.

In this study, we investigated the effect of the two flavonoids, baicalin (baicalein 7-O-$\beta$- d-glucuronic acid) and its aglycone, baicalein (5,6,7-trihydroxyflavone), after encapsulation into amorphous calcium polyphosphate (Ca-polyP) microparticles on mineralization of primary human osteoblasts (phOSB). Both flavonoids, which come from root extracts of Scutellaria baicalensis Georgi, are used in Traditional Chinese Medicine, and are nontoxic in cells up to a concentration of 3$\mu$g/ml. The morphogenetically active, energy-rich Ca-polyP particles with a stoichiometric P:Ca ratio of 1:2 are degraded by cellular alkaline phosphatase (ALP) to ortho-phosphate used for bone hydroxyapatite formation. Here we show that the flavone-loaded Ca-polyP microparticles are readily taken up by phOSB, resulting in the accumulation of polyP around the nuclei and the formation of intracellular vesicles containing the ALP. In addition, we demonstrate that baicalin/baicalein causes a rise of the intracellular calcium [Ca${}^{2+}$]_i a level which markedly is augmented after encapsulation into Ca-polyP, through activation of the phospholipase C. Moreover, both flavones, either alone or associated with Ca-polyP microparticles, upregulate the expression of the osteoblast calcium efflux channel, the plasma membrane Ca${}^{2+}$-ATPase (PMCA), while the expression of ALP, which promotes bone mineralization, is induced by Ca-polyP and by the flavones only if present in the Ca-polyP-microparticle-associated form. As a result, the extent of bone mineralization is markedly enhanced. Based on the two-armed activating function, new applications of baicalin/baicalein as a component of nutriceuticals for osteoporosis prevention or bone implants can be envisaged.

Abundant evidence supports the key role of ultraviolet radiation (UVR) in skin cancer development. The human skin, especially the epidermal layer, is the main defense against UV radiation. Baicalin is a major bioactive component of Scutellaria baicalensis Georgi, a plant which has been found to exhibit antitumor activity. The anticarcinogenic mechanism of baicalin is not completely understood. We have reported that baicalin inhibited UVB-induced photo-damage and apoptosis in HaCaT cells (human skin keratinocytes). The aim of the present study is to investigate the cellular gene targets responsible for baicalin’s antitumor activity by performing two-dimensional electrophoresis liquid chromatography-mass spectrometry/mass spectrometry (2-DE LC-MS/MS) with HaCaT cells following UVB and baicalin exposure. Two-DE for protein separation was performed, followed by matrix-assisted laser desorption/ionization mass spectrometry and database searches. Nucleophosmin (NPM)-specific siRNA was designed and synthesized, and the small interfering RNA was transfected into skin squamous cancer A431 cells to knockdown the NPM expression. Proliferation and cell cycle status were assessed by CCK8 and flow cytometric analyses, respectively. We have identified 38 protein spots that are differentially expressed in HaCaT cells exposed to baicalin and/or UVB irradiation These proteins are involved in detoxification, proliferation, metabolism, cytoskeleton and motility. In particular, we found several proteins that have been linked to tumor progression and resistance, such as NPM. Baicalin treatment reduced the cellular proliferation rate and induced arrest during the S-phase of the cell cycle in A431 cells. NPM1 silencing significantly enhanced the effect of baicalin. Our data indicated that baicalin results in the significant inhibition of tumor growth in the A431 cell line, which may be associated with the regulation of the NPM gene expression.

Scutellaria baicalensis (Huangqin in Chinese) is a major traditional Chinese medicine (TCM) herb, which has a long history of use in the treatment of a variety of symptoms correlated with cancer. In the past decade, the potential of S. baicalensis and single compounds derived from it as anticancer agents targeting various pathways has received extensive research attention. Specifically, the proliferation and metastases inhibiting properties of the single compounds in cancer have been studied; however, the underlying mechanisms remain unclear. This review summarizes the various mechanisms, pathways and molecular targets involved in the anticancer activity of S. baicalensis and its single compounds. However, the aim of this review is to provide a more thorough view of the last 10 years to link traditional use with modern research and to highlight recently discovered molecular mechanisms. Extracts and major flavonoids derived from S. baicalensis have been found to possess anticancer effects in multiple cancer cell lines both in vitro and in vivo. Further investigation is warranted to better understand the underlying mechanisms and to discover novel targets and cancer therapeutic drugs that may improve both the survival and quality of life of cancer patients.

Baicalin is the main active ingredient primary isolated from the Chinese herb, Scutellaria baicalensis Georgi. Although baicalin can induce M2 macrophage polarization, we still do not know the subtype of macrophages polarized by baicalin. In this study, we characterized that murine bone marrow derived macrophages induced by M-CSF can be further polarized into M2_C phenotype by baicalin. The signatures of M2_C macrophages for mRNA expression like interferon regulatory factor 4 (IRF4), interleukin-10 (IL-10), MERTK and PTX3 were up-regulated. Moreover, we observed the concomitantly decreasing of tumor necrosis factor alpha (TNF-$\alpha$), interferon regulatory factor 5 (IRF5), IL-6. In contrast, M2 macrophages polarized by IL-4 increased gene transcript of arginase-1 (Arg-1) and surface marker of CD206 indicates that their identity as M2_A rather than M2_C subtypes. Interestingly, the phagocytosis as well as efferocytosis activity were significantly enhanced in M2_C macrophage polarized by baicalin and these capacities were associated with the expression of MERTK receptor. Finally, we conclude that baicalin induced M2_C macrophages polarization with both elevations of efferocytosis and anti-inflammatory activity.

Baicalin is a flavonoid extracted from Scutellariae Radix and shows a variety of biological activities as reducing lipids, diminishing inflammation, and inhibiting bacterial infection. However, there is no report of baicalin against CVB3 infection. In this study, we found that baicalin can reduce viral titer in a dose-dependent manner in vitro at a dose with no direct virucidal effect. Moreover, we revealed that baicalin can also improve survival rate, reduce heart weight/body weight ratio, prevent virus replication, and relieve myocardial inflammation in the acute viral myocarditis mouse model induced by CVB3. Then, in order to explore the mechanism of baicalin inhibiting CVB3 replication, we respectively examined the expression of autophagosome marker LC3-II by Western blot, tested the concentration of free fatty acid (FFA) and cholesterol (CHO) by commercial kits, detected the mRNA levels of fatty acid synthase (Fasn) and acetyl coenzyme a carboxylase (ACC) by RT-PCR, and observed the lipid content of cells by fluorescence staining. The results showed that CVB3 infection increased autophagosome formation and lipid content in HeLa cells, but these changes were significantly blocked by baicalin. Finally, in order to confirm that baicalin inhibits viral replication and reduces autophagosome formation by reducing cellular lipids, we added exogenous palmitate to cell culture supernatants to promote intracellular lipid synthesis and found that palmitate did not alter LC3-II and CVB3/VP1 expression in HeLa cells with or without CVB3 infection. Interestingly, palmitate can reverse the inhibitory effect of baicalin on autophagosome formation and viral replication. In conclusion, our results indicated that lipids play an important role in CVB3 replication, and the effect of baicalin against CVB3 was associated with its ability to reduce cellular lipid synthesis to limit autophagosome formation.

Acute pancreatitis (AP) is a kind of reversible inflammatory process of the exocrine pancreas. During the process, systemic inflammatory syndromes are involved, which relates closely to inflammatory mediators. Baicalin is a type of flavone compound extracted from Scutellaria baicalensis Georgi and exhibits anti-inflammation effect in several cancers. In this study, baicalin displayed a suppressing role on IL-1$\beta$, TNF$\alpha$ and IL-6 in both cell and mice models. Necrosis was decreased in the baicalin treatment group and got a markedly lower pathological score. In this study, miR-15a is the core intermediate in baicalin regulation, which increased through baicalin treatment and protected pancreas cells and tissues, inhibiting the JNK signaling pathway by targeting MAP2K4. The long non-coding RNA MALAT1 is also a direct target of miR-15a and forms a competitive endogenous RNA (ceRNA) network with MAP2K4, which can be regulated by baicalin. In addition, upstream genes, including CDC42 and MAP3K1, were also regulated by baicalin, of which CDC42 was confirmed to form the second ceRNA network with MALAT1 and miR-15a. In conclusion, baicalin exhibits therapeutic activity towards AP by pumping up miR-15a level and inhibiting CDC42/MAP3K1, which affects AP as a brake by targeting MAP2K4 and inhibiting the JNK signaling pathway.

Baicalin was reported to facilitate the apoptosis of colon cells and inhibit tumor growth in vivo. This study aimed to explore the specific mechanism and function of baicalin on colon cells. Relative mRNA levels were tested via qPCR. Cell proliferation, viability, and cell cycle phases were evaluated using MTT, colony formation, and flow cytometry assays, respectively. The interaction between miR-139-3p and cyclin-dependent kinase 16 (CDK16) was measured via a dual-luciferase reporter assay. Immunohistochemistry was used to count the positivity cells in tumor tissues collected from treated xenografted tumor mice. The results showed that baicalin increased miR-139-3p expression while also decreasing CDK16 levels, blocking the cell cycle, and inhibiting cell proliferation in colon cancer cells. miR-139-3p silencing or CDK16 overexpression abolished the inhibitory effects of baicalin on colon cancer proliferation. miR-139-3p directly targeted and interacted with CDK16 at the cellular level. The protective functions of miR-139-3p knockdown on tumor cells were abrogated by silencing CDK16. The combination of baicalin treatment and CDK16 knockdown further inhibited tumor growth of xenografted tumor mice compared with the groups injected with only sh-CDK16 or baicalin in vivo. In conclusion, baicalin inhibited colon cancer growth by modulating the miR-139-3p/CDK16 axis.

Ischemic stroke is a serious health hazard that lacks effective treatment strategies. This study aims to investigate baicalin’s effect on tight junctions and immune cell infiltration after ischemic stroke injury. Rat brain microvascular endothelial cells (BMECs) were treated with OGD/R to establish an in vitro model. Caspase-3, Bax, Bcl-2, zonula occludens-1 (ZO-1), occludin, claudin-5, tumor necrosis factor (TNF)-$\alpha$, interleukin (IL)-6, inducible nitric oxide synthase (iNOS), Toll-like receptor (TLR) 2, TLR4, and nuclear factor-kappa B (NF-$\kappa$B) expressions were detected using qRT-PCR and western blotting. ZO-1, TNF-$\alpha$, iNOS, IL6, CD31, and ZO-1 expressions were examined using immunofluorescence. A tube formation assay was performed to measure angiogenesis. An ischemia-reperfusion model in rats was established by middle cerebral artery occlusion. The infarct volume was observed using 2,3,5-triphenyltetrazolium chloride staining. TNF-$\alpha$, iNOS, and IL6 levels in the serum were tested using ELISA. Flow cytometry was performed to examine immune cell inflammatory infiltration. Baicalin had no significant effect on the proliferation of normal BMECs. Baicalin inhibited apoptosis, protected against tight junction injury, and alleviated the inflammatory response in OGD/R-induced BMECs and IR rats, with the highest dose (25$\mu$g/mL) exerting a superior effect. Baicalin decreased the neurological function score, infarct volume, and brain water content, relieved brain morphological changes, and inhibited immune cell infiltration in vivo. In conclusion, baicalin could reduce BMECs apoptosis, protect tight junctions, and resist immune cell infiltration, thereby alleviating ischemic stroke. Our findings potentially provide a novel treatment strategy for ischemic stroke.

Hemorrhagic shock (HS) is defined as a reduction in tissue oxygenation and organ dysfunction due to severe blood loss. Lung injury is a frequent complication of HS. Baicalin, isolated from Radix Scutellariae, has been reported to profile the antitumor, anti-oxidative, anti-inflammatory, and antibacterial roles in various pathological processes. Nevertheless, the effects of baicalin on HS-induced lung injury are unclear. This study aims to examine the therapeutic effects of baicalin on lung injury. We first established the lung injury rat models by withdrawing blood in the femoral artery followed by resuscitation. A pathological analysis showed that HS-administrated rats presented severe capillary leakage and pulmonary edema, while baicalin therapy alleviated the symptoms. Baicalin therapy reduced the number of macrophages and neutrophils in bronchoalveolar lavage fluid and decreased the expression and activity of myeloperoxidase (neutrophile infiltration marker) in the lung tissues of HS rats, indicating that baicalin alleviated HS-induced infiltration of inflammatory cells. The secretion of inflammatory cytokines, including interleukin (IL)-1$\beta$, IL-6, IL-18, and tumor necrosis factor $\alpha$ (TNF-$\alpha$), as well as the activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing-3 (NLRP3) inflammasome, were inhibited by baicalin administration. Furthermore, we found that the NF-$\kappa$B pathway, a canonical pro-inflammatory pathway, was also blocked after treatment with baicalin in HS-evoked rats, as indicated by the decreased expression of p65 and p65 phosphorylation in the lung tissues. In summary, we infer that baicalin may exert a protective role in HS-induced lung injury by suppressing the activation of NLRP3 inflammasome via the NF-$\kappa$B pathway.

Scutellaria baicalensis (Huangqin in Chinese) is a major traditional Chinese medicine (TCM) herb, which has a long history of use in the treatment of a variety of symptoms correlated with cancer. In the past decade, the potential of S. baicalensis and single compounds derived from it as anticancer agents targeting various pathways has received extensive research attention. Specifically, the proliferation and metastases inhibiting properties of the single compounds in cancer have been studied; however, the underlying mechanisms remain unclear. This review summarizes the various mechanisms, pathways and molecular targets involved in the anticancer activity of S. baicalensis and its single compounds. However, the aim of this review is to provide a more thorough view of the last 10 years to link traditional use with modern research and to highlight recently discovered molecular mechanisms. Extracts and major flavonoids derived from S. baicalensis have been found to possess anticancer effects in multiple cancer cell lines both in vitro and in vivo. Further investigation is warranted to better understand the underlying mechanisms and to discover novel targets and cancer therapeutic drugs that may improve both the survival and quality of life of cancer patients.