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Berberine
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Product Name Berberine
Price: $40 / 20mg
CAS No.: 2086-83-1
Catalog No.: CFN98049
Molecular Formula: C20H18NO4
Molecular Weight: 336.4 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Yellow powder
Source: The herbs of Coptis chinensis Franch.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Berberine has neuroprotective, antidepressant, antineoplastic, and anti- fibrosis activities; it is a potent oral hypoglycemic agent with beneficial effects on lipid metabolism, it may as a broad-spectrum anti-microbial medicine, a complementary therapeutic agent for HIV/AIDS; it also may be one of the targeted therapeutic agents that can restore barrier function in intestinal disease states.Berberine is used in histology for staining heparin in mast cells. As a natural dye, berberine has a colour index of 75160.
Targets: ROS | COX | AMPK | Bcl-2/Bax | Caspase | TGF-β/Smad | ROS | GLUT | Akt | GSK-3 | Beta Amyloid
In vitro:
Mol Med Rep. 2014 Oct;10(4):1734-8.
Berberine induces apoptosis and DNA damage in MG‑63 human osteosarcoma cells.[Pubmed: 25050485]
Berberine, an isoquinoline alkaloid extracted from the dry root of Coptidis Rhizoma, has been found to exhibit marked anticancer effects on a panel of established cancer cells. Among the human osteosarcoma lines treated, MG‑63 cells were found to be the most sensitive. The present study investigated the potential genotoxic effect of Berberine on MG‑63 human osteosarcoma cells.
METHODS AND RESULTS:
The effect of Berberine on cell viability was determined using a 3-(4,5-dimethylthiazol-2-yl)-2,5‑diphenyltetrazolium bromide assay and cell apoptosis was analyzed by flow cytometry and a DNA ladder assay. γH2AX focus formation was used to detect DNA damage in MG-63 cells. Berberine induced a significant increase in apoptosis in MG-63 cells in a concentration- and time-dependent manner, as determined by DNA fragmentation analysis and flow cytometry. Furthermore, Berberine induced significant concentration- and time-dependent increases in DNA damage compared with that in the negative control.
CONCLUSIONS:
In conclusion, these observations indicated that Berberine induced apoptosis and DNA damage in MG‑63 cells.
In vivo:
Biochem Biophys Res Commun. 2015 Mar 20;458(4):796-801.
Berberine improves endothelial function by inhibiting endoplasmic reticulum stress in the carotid arteries of spontaneously hypertensive rats.[Pubmed: 25686503]
Activation of endoplasmic reticulum (ER) stress in endothelial cells leads to increased oxidative stress and often results in cell death, which has been implicated in hypertension. The present study investigated the effects of Berberine, a botanical alkaloid purified from Coptidis rhizoma, on ER stress in spontaneously hypertensive rats (SHRs) and the underling mechanism.
METHODS AND RESULTS:
Isolated carotid arteries from normotensive WKYs and SHRs were suspended in myograph for isometric force measurement. Protein phosphorylations and expressions were determined by Western blotting. Reactive oxygen species (ROS) level was measured by DHE staining. SHR carotid arteries exhibited exaggerated acetylcholine-triggered endothelium-dependent contractions (EDCs) and elevated ROS accumulation compared with WKY arteries. Moreover, Western blot analysis revealed the reduced AMPK phosphorylation, increased eIF2α phosphorylation, and elevated levels of ATF3, ATF6, XBP1 and COX-2 in SHR carotid arteries while these pathological alterations were reversed by 12 h-incubation with Berberine. Furthermore, AMPK inhibitor compound C or dominant negative AMPK adenovirus inhibited the effects of Berberine on above-mentioned marker proteins and EDCs. More importantly, ROS scavengers, tempol and tiron plus DETCA, or ER stress inhibitors, 4-PBA and TUCDA normalized the elevated levels of ROS and COX-2 expression, and attenuated EDCs in SHR arteries.
CONCLUSIONS:
Taken together, the present results suggest that Berberine reduces EDCs likely through activating AMPK, thus inhibiting ER stress and subsequently scavenging ROS leading to COX-2 down-regulation in SHR carotid arteries. The present study thus provides additional insights into the vascular beneficial effects of Berberine in hypertension.
Diabetes. 2006 Aug;55(8):2256-64.
Berberine, a natural plant product, activates AMP-activated protein kinase with beneficial metabolic effects in diabetic and insulin-resistant states.[Pubmed: 16873688 ]
Berberine has been shown to have antidiabetic properties, although its mode of action is not known. Here, we have investigated the metabolic effects of Berberine in two animal models of insulin resistance and in insulin-responsive cell lines.
METHODS AND RESULTS:
Berberine reduced body weight and caused a significant improvement in glucose tolerance without altering food intake in db/db mice. Similarly, Berberine reduced body weight and plasma triglycerides and improved insulin action in high-fat-fed Wistar rats. Berberine downregulated the expression of genes involved in lipogenesis and upregulated those involved in energy expenditure in adipose tissue and muscle. Berberine treatment resulted in increased AMP-activated protein kinase (AMPK) activity in 3T3-L1 adipocytes and L6 myotubes, increased GLUT4 translocation in L6 cells in a phosphatidylinositol 3' kinase-independent manner, and reduced lipid accumulation in 3T3-L1 adipocytes.
CONCLUSIONS:
These findings suggest that Berberine displays beneficial effects in the treatment of diabetes and obesity at least in part via stimulation of AMPK activity.
Neurobiol Aging. 2012 Dec;33(12):2903-19.
Berberine ameliorates β-amyloid pathology, gliosis, and cognitive impairment in an Alzheimer's disease transgenic mouse model.[Pubmed: 22459600 ]
The accumulation of β-amyloid (Aβ) peptide derived from abnormal processing of amyloid precursor protein (APP) is a common pathological hallmark of Alzheimer's disease (AD) brains.
METHODS AND RESULTS:
In this study, we evaluated the therapeutic effect of Berberine (BBR) extracted from Coptis chinensis Franch, a Chinese medicinal herb, on the neuropathology and cognitive impairment in TgCRND8 mice, a well established transgenic mouse model of AD. Two-month-old TgCRND8 mice received a low (25 mg/kg per day) or a high dose of BBR (100 mg/kg per day) by oral gavage until 6 months old. BBR treatment significantly ameliorated learning deficits, long-term spatial memory retention, as well as plaque load compared with vehicle control treatment. In addition, enzyme-linked immunosorbent assay (ELISA) measurement showed that there was a profound reduction in levels of detergent-soluble and -insoluble β-amyloid in brain homogenates of BBR-treated mice. Glycogen synthase kinase (GSK)3, a major kinase involved in APP and tau phosphorylation, was significantly inhibited by BBR treatment. We also found that BBR significantly decreased the levels of C-terminal fragments of APP and the hyperphosphorylation of APP and tau via the Akt/glycogen synthase kinase 3 signaling pathway in N2a mouse neuroblastoma cells stably expressing human Swedish mutant APP695 (N2a-SwedAPP).
CONCLUSIONS:
Our results suggest that BBR provides neuroprotective effects in TgCRND8 mice through regulating APP processing and that further investigation of the BBR for therapeutic use in treating AD is warranted.
Front Pharmacol . 2021 Jun 17;12:632201.
Berberine Sensitizes Human Hepatoma Cells to Regorafenib via Modulating Expression of Circular RNAs[Pubmed: 34220494]
Regorafenib resistance is a key limiting factor in the treatment of advanced hepatocellular carcinoma (HCC). Increasing evidence has demonstrated that Berberine (BBR) can synergistically enhance the therapeutic effect of various chemotherapeutic agents. However, the contribution of BBR on regorafenib therapy remains unclear. The purpose of this study was to explore the combined treatment effect of Berberine and regorafenib in HCC. We found that BBR enhanced the cytotoxicity of regorafenib in HCC cells. Compared with regorafenib alone, the combined treatment of BBR and regorafenib significantly inhibited the proliferation of HCC cells and induced cellular apoptosis. Meanwhile, the combined treatment group with BBR (10mg/kg/day) and regorafenib (5mg/kg/day) had a dramatic inhibitory effect on the growth of HCC xenograft tumors in nude mice. The increased apoptosis of xenograft tumors was seen in the combined treatment group. Moreover, a comprehensive circular RNA sequencing was performed to identify differentially expressed circRNAs in HCC cells after exposure to 100μM BBR and 5μM regorafenib. The volcano plot and scatter plot analyses revealed that there were 58 up-regulated and 19 down-regulated differentially expressed circRNAs between the combination treatment and control groups. Among them, the expression of hsa_circ_0032029 and hsa_circ_0008928 were up-regulated in HCC cells after treatment with 100μM BBR and 5μM regorafenib. Taken together, this study demonstrated that BBR enhanced the anti-HCC effect of regorafenib both in vitro and in vivo. The synergistic anti-tumor effect of BBR and regorafenib might be related to the up-regulation of hsa_circ_0032029 and hsa_circ_0008928 in HCC cells.
Berberine Description
Source: The herbs of Coptis chinensis Franch.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

Cell. 2018 Jan 11;172(1-2):249-261.e12.
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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.9727 mL 14.8633 mL 29.7265 mL 59.453 mL 74.3163 mL
5 mM 0.5945 mL 2.9727 mL 5.9453 mL 11.8906 mL 14.8633 mL
10 mM 0.2973 mL 1.4863 mL 2.9727 mL 5.9453 mL 7.4316 mL
50 mM 0.0595 mL 0.2973 mL 0.5945 mL 1.1891 mL 1.4863 mL
100 mM 0.0297 mL 0.1486 mL 0.2973 mL 0.5945 mL 0.7432 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Cell Research:
J Med Food. 2014 Sep;17(9):955-62.
Synergistic inhibitory effect of berberine and d-limonene on human gastric carcinoma cell line MGC803.[Pubmed: 25045784]
This study aims at evaluating the anticancer effects of Berberine hydrochloride (Berberine) and d-limonene, alone and in combination, on human gastric carcinoma cell line MGC803 to determine whether Berberine and d-limonene work synergistically and elucidate their mechanisms. MGC803 cells were treated with Berberine and d-limonene, alone and in combination, for 24-48 h.
METHODS AND RESULTS:
The inhibitory effects of these drugs on growth were determined by MTT assay. The combination index and drug reduction index were calculated with the Chou-Talalay method based on the median-effect principle. Flow cytometry and laser scanning confocal microscopy were employed to evaluate the effects of both drugs on cell-cycle perturbation and apoptosis, generation of reactive oxygen species (ROS), mitochondrial membrane potential, and expression of Bcl-2 and caspase-3 in MGC803 cells. Berberine or d-limonene alone can inhibit the growth of MGC803 cells in a dose- and time-dependent manner. Berberine and d-limonene at a combination ratio of 1:4 exhibited a synergistic effect on anti-MGC803 cells. The two drugs distinctly induced intracellular ROS generation, reduced the mitochondrial transmembrane potential (ΔΨm), enhanced the expression of caspase-3, and decreased the expression of Bcl-2. The combination of Berberine and d-limonene showed more remarkable effects compared with drugs used singly in MGC803 cells.
CONCLUSIONS:
The combination of Berberine and d-limonene exerted synergistic anticancer effects on MGC803 cells by cell-cycle arrest, ROS production, and apoptosis induction through the mitochondria-mediated intrinsic pathway.
Animal Research:
Nephrology (Carlton). 2014 Sep;19(9):542-51.
Berberine ameliorates renal interstitial fibrosis induced by unilateral ureteral obstruction in rats.[Pubmed: 24754438]
To investigate the potential effects of Berberine on renal interstitial fibrosis (RIF) of obstructed kidneys in a unilateral ureteral obstruction (UUO) rat model.
METHODS AND RESULTS:
Forty-eight rats were randomly divided into three groups: sham-operated, vehicle-treated UUO, and Berberine-treated UUO. Rats were gavaged with Berberine (200 mg/kg per day) or vehicle. Eight randomly chosen rats in each group were kiled and specimens were collected at day 14 after UUO. Physiological parameters and histological changes were assessed, RIF was evaluated using Masson's trichrome and Sirius red staining, oxidative stress and inflammation markers were determined, transforming growth factor β1 (TGF-β1), phosphorylated Smad3 (pSmad3) and α-smooth muscle actin (α-SMA) were measured using immunohistochemistry or western blotting analysis. The obstruction was relieved at day 14 by percutaneous nephrostomy in the remaining UUO rats. The resistive index of left kidneys was undertaken by coloured Doppler flow imaging at day 14 before nephrostomy and day 7 after the relief. Berberine treatment significantly attenuated RIF induced by UUO. The UUO-induced reduction in kidney superoxide dismutase and catalase activities increased, whereas elevated kidney malondialdehyde level markedly decreased. Berberine treatment significantly ameliorated UUO-induced inflammation, and decreased TGF-β1, pSmad3 and α-SMA expression of UUO kidneys. Moreover, Berberine treatment significantly suppressed the increase of resistive index compared with UUO group at day 14 after UUO as well as day 7 after the relief of obstruction.
CONCLUSIONS:
Berberine treatment ameliorates RIF in a UUO rat model by inhibition of oxidative stress, inflammatory responses, and TGF-β1/pSmad3 signalling.
Mol Pharmacol. 2014 Dec;86(6):609-23.
Berberine reverses epithelial-to-mesenchymal transition and inhibits metastasis and tumor-induced angiogenesis in human cervical cancer cells.[Pubmed: 25217495]
Metastasis is the most common cause of cancer-related death in patients, and epithelial-to-mesenchymal transition (EMT) is essential for cancer metastasis, which is a multistep complicated process that includes local invasion, intravasation, extravasation, and proliferation at distant sites. When cancer cells metastasize, angiogenesis is also required for metastatic dissemination, given that an increase in vascular density will allow easier access of tumor cells to circulation, and represents a rational target for therapeutic intervention. Berberine has several anti-inflammation and anticancer biologic effects.
METHODS AND RESULTS:
In this study, we provided molecular evidence that is associated with the antimetastatic effect of Berberine by showing a nearly complete inhibition on invasion (P < 0.001) of highly metastatic SiHa cells via reduced transcriptional activities of matrix metalloproteinase-2 and urokinase-type plasminogen activator. Berberine reversed transforming growth factor-β1-induced EMT and caused upregulation of epithelial markers such as E-cadherin and inhibited mesenchymal markers such as N-cadherin and snail-1. Selective snail-1 inhibition by snail-1-specific small interfering RNA also showed increased E-cadherin expression in SiHa cells. Berberine also reduced tumor-induced angiogenesis in vitro and in vivo.
CONCLUSIONS:
Importantly, an in vivo BALB/c nude mice xenograft model and tail vein injection model showed that Berberine treatment reduced tumor growth and lung metastasis by oral gavage, respectively. Taken together, these findings suggested that Berberine could reduce metastasis and angiogenesis of cervical cancer cells, thereby constituting an adjuvant treatment of metastasis control.
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