Sophocarpine

CAS# 145572-44-7

Sophocarpine

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Quality Control of Sophocarpine

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Chemical structure

Sophocarpine

3D structure

Chemical Properties of Sophocarpine

Cas No. 145572-44-7 SDF Download SDF
PubChem ID 115269 Appearance White crystalline
Formula C15H22N2O M.Wt 246.35
Type of Compound Nitrogen-containing Compounds Storage Desiccate at -20°C
Synonyms 6483-15-4;13,14-Didehydromatrine
Solubility Soluble to 49 mg/mL (198.9 mM) in DMSO
Chemical Name (1R,2R,9S,17S)-7,13-diazatetracyclo[7.7.1.02,7.013,17]heptadec-4-en-6-one
SMILES C1CC2CN3C(CC=CC3=O)C4C2N(C1)CCC4
Standard InChIKey AAGFPTSOPGCENQ-JLNYLFASSA-N
Standard InChI InChI=1S/C15H22N2O/c18-14-7-1-6-13-12-5-3-9-16-8-2-4-11(15(12)16)10-17(13)14/h1,7,11-13,15H,2-6,8-10H2/t11-,12+,13+,15-/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Sophocarpine

The herb of Sophora alopecuroidos L.

Biological Activity of Sophocarpine

DescriptionSophocarpine has anti-cachectic, anti-inflammatory, and neuroprotective effects. It has significant antivirus effects against coxsackievirus B3 and therapeutic effects for viral myocarditis in clinical, can ameliorate the ischemic injury induced by transient focal cerebral ischemia in rats, and may be a potential chemotherapeutic agent for chronic liver diseases. Sophocarpine inhibited the expression of TNF-alpha, IL-6, JNK, iNOS, COX-2, p38 MAPK, NF-κB, TLR4, and activated signaling pathway of AMPK.
TargetsTGF-β/Smad | TLR | ERK | JNK | p38MAPK | IkB | AMPK | NF-kB | NOS | COX | TNF-α | IL Receptor | IKK
In vitro

Sophocarpine alleviates hepatocyte steatosis through activating AMPK signaling pathway.[Pubmed: 23395669]

Toxicol In Vitro. 2013 Apr;27(3):1065-71.

Sophocarpine, an effective compound derived from foxtail-like sophora herb and seed, has been reported that it can alleviate non-alcoholic steatohepatitis (NASH) in rats and affect adipocytokine synthesis. Meanwhile, adipocytokines could adjust hepatic lipid metabolism through AMPK signaling pathway.
METHODS AND RESULTS:
In the work presented here, primary hepatocytes were isolated from specific pathogen-free male SD rats and incubated with 200 μmol/L oleic acid for 24h to induce steatotic model, then treated with Sophocarpine for 72 h. Oil red staining was performed to evaluate steatosis, total RNA and protein of primary hepatocytes were extracted for real-time RT-PCR and western blot analysis. A cluster of aberrances were observed in the model group, including hepatocyte steatosis, increased leptin and decreased adiponectin mRNA expressions. While Sophocarpine treatment resulted in: significant improvement of steatosis (>50% decrease), decrease of leptin expression (<0.57-fold) and increase of adiponectin expression (>1.48-fold). Moreover, compared with the model group, Sophocarpine could significantly increase P-AMPKα (>5.82-fold), AMPKα (>1.29-fold) and ACC (>3.27-fold) protein expressions, and reduce P-ACC (<0.30-fold) and HNF-4α (<0.20-fold) protein expression. The mRNA expression of Srebp-1c was downregulated significantly simultaneously (<0.68-fold).
CONCLUSIONS:
We concluded that Sophocarpine could alleviate hepatocyte steatosis and the potential mechanism might be the activated signaling pathway of AMPK.

Anti-inflammatory effects of sophocarpine in LPS-induced RAW 264.7 cells via NF-κB and MAPKs signaling pathways.[Pubmed: 21978812]

Toxicol In Vitro. 2012 Feb;26(1):1-6.

Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides L. Our previous studies have showed that Sophocarpine exerts anti-inflammatory activity in animal models.
METHODS AND RESULTS:
In the present study, anti-inflammatory mechanisms of Sophocarpine were investigated in lipopolysaccharide (LPS)-induced responses in RAW 264.7 cells. Furthermore, the cytotoxicity of Sophocarpine was tested. The results indicated that Sophocarpine could increase the LDH level and inhibit cell viability up to 800μg/ml, and which was far higher than that of the plasma concentration of Sophocarpine in clinical effective dosage. The results also demonstrated that Sophocarpine (50 and 100μg/ml) suppressed LPS-stimulated NO production and pro-inflammatory cytokines secretion, including tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6). These were associated with the decrease of the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Furthermore, Sophocarpine inhibited LPS-mediated nuclear factor-κB (NF-κB) activation via the prevention of inhibitor κB (IκB) phosphorylation. Sophocarpine had no effect on the LPS-induced phosphorylation of extracellular signal-regulated kinase 1/2 (Erk1/2), whereas it attenuated the phosphorylation of p38 mitogen-activated protein (MAP) kinase and c-Jun NH(2)-terminal kinase (JNK).
CONCLUSIONS:
Our data suggested that Sophocarpine exerted anti-inflammatory activity in vitro, and it might attribute to the inhibition of iNOS and COX-2 expressions via down-regulation of the JNK and p38 MAP kinase signal pathways and inhibition of NF-κB activation.

In vivo

Neuroprotective effect of sophocarpine against transient focal cerebral ischemia via down-regulation of the acid-sensing ion channel 1 in rats.[Pubmed: 21232529]

Brain Res. 2011 Mar 25;1382:245-51.

Sophocarpine, one of the major alkaloid compounds isolated from Sophora pachycarpa, is highly valued and important in traditional Chinese medicine. In the present study, we aimed to explore the possible mechanisms underlying Sophocarpine-mediated neuroprotection against transient focal cerebral ischemia.
METHODS AND RESULTS:
Sophocarpine (5, 10, or 20mg/kg) was given 30min before focal ischemia was induced in rats by occlusion of the middle cerebral artery. After Sophocarpine treatment, the total infarct volume was significantly decreased in comparison to the ischemia-reperfusion values. The results of a neurological evaluation were significantly improved in the Sophocarpine treated group when compared to controls. The number of TUNEL-positive cells was significantly reduced compared to the untreated ischemic group. Results of Western blotting and immunohistochemical staining indicated that pretreatment with Sophocarpine down-regulated the expression of acid-sensing ion channel 1 (ASIC1) in the ischemic cortex.
CONCLUSIONS:
These results suggest that Sophocarpine ameliorated the ischemic injury induced by transient focal cerebral ischemia in rats and that this neuroprotective effect might be related to the anti-ASIC1 channel and anti-apoptotic action of Sophocarpine.

Protocol of Sophocarpine

Cell Research

Sophocarpine and matrine inhibit the production of TNF-alpha and IL-6 in murine macrophages and prevent cachexia-related symptoms induced by colon26 adenocarcinoma in mice.[Pubmed: 18775799 ]

Int Immunopharmacol. 2008 Dec 20;8(13-14):1767-72.

The present study aims to access the effects of sophora alkaloids on the production of pro-inflammatory cytokines and evaluate their therapeutic efficiency on cachexia.
METHODS AND RESULTS:
The comparative study showed that all sophora alkaloids tested here, including matrine, oxymatrine, Sophocarpine, sophoramine, and sophoridine, inhibited TNF-alpha and IL-6 production in both RAW264.7 cells and murine primary macrophages, and Sophocarpine showed the most potent inhibitory effect among them. Quantification of TNF-alpha and IL-6 mRNA in RAW264.7 cells by real-time RT-PCR revealed that both Sophocarpine and matrine suppressed TNF-alpha and IL-6 expression and Sophocarpine has stronger suppressing potency than matrine. Inoculation (s.c.) of colon26 adenocarcinoma cells into BALB/c mice induced cachexia, as evidenced by progressive weight loss, reduction in food intake, wasting of gastrocnemius muscle and epididymal fat, and increase in serum levels of TNF-alpha and IL-6. Administration of 50 mg/kg/d Sophocarpine or matrine for 5 days from the onset of cachexia did not inhibit the tumor growth but resulted in attenuation of cachexia symptoms. Furthermore, Sophocarpine and matrine decreased the serum levels of TNF-alpha and IL-6, and Sophocarpine showed a better therapeutic effect than matrine.
CONCLUSIONS:
These results suggest that Sophocarpine and matrine exert anti-cachectic effects probably through inhibition of TNF-alpha and IL-6.

Animal Research

Sophocarpine attenuates liver fibrosis by inhibiting the TLR4 signaling pathway in rats.[Pubmed: 24587659]

World J Gastroenterol. 2014 Feb 21;20(7):1822-32.

To explore the effect of Sophocarpine on experimental liver fibrosis and the potential mechanism involved.
METHODS AND RESULTS:
Sophocarpine was injected intraperitoneally in two distinct rat hepatic fibrosis models induced either by dimethylnitrosamine or bile duct ligation. Masson's trichrome staining, Sirius red staining and hepatic hydroxyproline level were used for collagen determination. Primary hepatic stellate cells (HSCs) were isolated and treated with different concentrations of Sophocarpine. Real-time reverse transcription-polymerase chain reaction was used to detect the mRNA levels of fibrotic markers and cytokines. The expression of pathway proteins was measured by Western blot. The Cell Counting Kit-8 test was used to detect the proliferation rate of activated HSCs treated with a gradient concentration of Sophocarpine. Sophocarpine decreased serum levels of aminotransferases and total bilirubin in rats under chronic insult. Moreover, administration of Sophocarpine suppressed extracellular matrix deposition and prevented the development of hepatic fibrosis. Furthermore, Sophocarpine inhibited the expression of α-smooth muscle actin (SMA), interleukin (IL)-6, transforming growth factor-β1 (TGF-β1), Toll-like receptor 4 (TLR4), and extracellular-related kinase (ERK) in rats. Sophocarpine also down-regulated the mRNA expression of α-SMA, collagen I, collagen III, TGF-β1, IL-6, tumor necrosis factor-α and monocyte chemoattractant protein-1, and decreased protein levels of TLR4, p-ERK, p-JNK, p-P38 and p-IKK in vitro after Lipopolysaccharide induction. In addition, Sophocarpine inhibited the proliferation of HSCs accompanied by a decrease in the expression of Cyclin D1. The protein level of proliferating cell nuclear antigen was decreased in activated HSCs following a gradient concentration of Sophocarpine.
CONCLUSIONS:
Sophocarpine can alleviate liver fibrosis mainly by inhibiting the TLR4 pathway. Sophocarpine may be a potential chemotherapeutic agent for chronic liver diseases.

Sophocarpine Dilution Calculator

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Preparing Stock Solutions of Sophocarpine

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.0593 mL 20.2963 mL 40.5927 mL 81.1853 mL 101.4816 mL
5 mM 0.8119 mL 4.0593 mL 8.1185 mL 16.2371 mL 20.2963 mL
10 mM 0.4059 mL 2.0296 mL 4.0593 mL 8.1185 mL 10.1482 mL
50 mM 0.0812 mL 0.4059 mL 0.8119 mL 1.6237 mL 2.0296 mL
100 mM 0.0406 mL 0.203 mL 0.4059 mL 0.8119 mL 1.0148 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Sophocarpine

Sophocarpine administration preserves myocardial function from ischemia-reperfusion in rats via NF-kappaB inactivation.[Pubmed:21459139]

J Ethnopharmacol. 2011 Jun 1;135(3):620-5.

ETHNOPHARMACOLOGICAL RELEVANCE: Sophora alopecuroides L. (the clinical usefulness of compound Kudouzi injection) has been used mainly for the treatment of fever, inflammation, edema and pain. Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides L. Sophocarpine injection (called the Kangke injection) has been demonstrated to have significant antivirus effects against coxsackievirus B3 and therapeutic effects for viral myocarditis in clinical. AIM OF THE STUDY: The present study was to evaluate the protective effect of Sophocarpine on the inhibition of NF-kappaB (NF-kappaB) and effect on inflammatory markers during myocardial ischemia-reperfusion (I/R) injury in rat. MATERIALS AND METHODS: Myocardial I/R injury was induced by the occlusion of left anterior descending coronary artery for 30 min followed by reperfusion for 2 h. 2 h after reperfusion was established, the hemodynamics and infarct size were examined. Blood samples were collected for biochemical analysis. Expression of NF-kappaB and mitogen-activated protein kinases (MAPKs) in ischemic myocardial tissue were assayed by western blot. RESULTS: Administration of Sophocarpine significantly improved cardiac function and reduced infarct size in I/R rat heart in vivo. Furthermore, Sophocarpine ameliorated the contents of inflammatory mediators (tumor necrosis factor-alpha, TNF-alpha; interleukin-6, IL-6; IL-10), neutrophil infiltration and myeloperoxidase (MPO) activity. Interestingly, Sophocarpine also significantly inhibited translocation of NF-kappaB, which was associated with attenuated phosphorylations of p38 and c-Jun NH2-terminal protein kinase (JNK). CONCLUSIONS: Inflammatory mediators, infiltration of neutrophil, and MPO were ameliorated via down-regulation of JNK and p38, and inactivation of NF-kappaB. This might be one of the important mechanisms of Sophocarpine that protected myocardial injury from I/R.

Anti-inflammatory effects of sophocarpine in LPS-induced RAW 264.7 cells via NF-kappaB and MAPKs signaling pathways.[Pubmed:21978812]

Toxicol In Vitro. 2012 Feb;26(1):1-6.

Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides L. Our previous studies have showed that Sophocarpine exerts anti-inflammatory activity in animal models. In the present study, anti-inflammatory mechanisms of Sophocarpine were investigated in lipopolysaccharide (LPS)-induced responses in RAW 264.7 cells. Furthermore, the cytotoxicity of Sophocarpine was tested. The results indicated that Sophocarpine could increase the LDH level and inhibit cell viability up to 800mug/ml, and which was far higher than that of the plasma concentration of Sophocarpine in clinical effective dosage. The results also demonstrated that Sophocarpine (50 and 100mug/ml) suppressed LPS-stimulated NO production and pro-inflammatory cytokines secretion, including tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6). These were associated with the decrease of the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Furthermore, Sophocarpine inhibited LPS-mediated nuclear factor-kappaB (NF-kappaB) activation via the prevention of inhibitor kappaB (IkappaB) phosphorylation. Sophocarpine had no effect on the LPS-induced phosphorylation of extracellular signal-regulated kinase 1/2 (Erk1/2), whereas it attenuated the phosphorylation of p38 mitogen-activated protein (MAP) kinase and c-Jun NH(2)-terminal kinase (JNK). Our data suggested that Sophocarpine exerted anti-inflammatory activity in vitro, and it might attribute to the inhibition of iNOS and COX-2 expressions via down-regulation of the JNK and p38 MAP kinase signal pathways and inhibition of NF-kappaB activation.

Neuroprotective effect of sophocarpine against transient focal cerebral ischemia via down-regulation of the acid-sensing ion channel 1 in rats.[Pubmed:21232529]

Brain Res. 2011 Mar 25;1382:245-51.

Sophocarpine, one of the major alkaloid compounds isolated from Sophora pachycarpa, is highly valued and important in traditional Chinese medicine. In the present study, we aimed to explore the possible mechanisms underlying Sophocarpine-mediated neuroprotection against transient focal cerebral ischemia. Sophocarpine (5, 10, or 20mg/kg) was given 30min before focal ischemia was induced in rats by occlusion of the middle cerebral artery. After Sophocarpine treatment, the total infarct volume was significantly decreased in comparison to the ischemia-reperfusion values. The results of a neurological evaluation were significantly improved in the Sophocarpine treated group when compared to controls. The number of TUNEL-positive cells was significantly reduced compared to the untreated ischemic group. Results of Western blotting and immunohistochemical staining indicated that pretreatment with Sophocarpine down-regulated the expression of acid-sensing ion channel 1 (ASIC1) in the ischemic cortex. These results suggest that Sophocarpine ameliorated the ischemic injury induced by transient focal cerebral ischemia in rats and that this neuroprotective effect might be related to the anti-ASIC1 channel and anti-apoptotic action of Sophocarpine.

Sophocarpine attenuates liver fibrosis by inhibiting the TLR4 signaling pathway in rats.[Pubmed:24587659]

World J Gastroenterol. 2014 Feb 21;20(7):1822-32.

AIM: To explore the effect of Sophocarpine on experimental liver fibrosis and the potential mechanism involved. METHODS: Sophocarpine was injected intraperitoneally in two distinct rat hepatic fibrosis models induced either by dimethylnitrosamine or bile duct ligation. Masson's trichrome staining, Sirius red staining and hepatic hydroxyproline level were used for collagen determination. Primary hepatic stellate cells (HSCs) were isolated and treated with different concentrations of Sophocarpine. Real-time reverse transcription-polymerase chain reaction was used to detect the mRNA levels of fibrotic markers and cytokines. The expression of pathway proteins was measured by Western blot. The Cell Counting Kit-8 test was used to detect the proliferation rate of activated HSCs treated with a gradient concentration of Sophocarpine. RESULTS: Sophocarpine decreased serum levels of aminotransferases and total bilirubin in rats under chronic insult. Moreover, administration of Sophocarpine suppressed extracellular matrix deposition and prevented the development of hepatic fibrosis. Furthermore, Sophocarpine inhibited the expression of alpha-smooth muscle actin (SMA), interleukin (IL)-6, transforming growth factor-beta1 (TGF-beta1), Toll-like receptor 4 (TLR4), and extracellular-related kinase (ERK) in rats. Sophocarpine also down-regulated the mRNA expression of alpha-SMA, collagen I, collagen III, TGF-beta1, IL-6, tumor necrosis factor-alpha and monocyte chemoattractant protein-1, and decreased protein levels of TLR4, p-ERK, p-JNK, p-P38 and p-IKK in vitro after Lipopolysaccharide induction. In addition, Sophocarpine inhibited the proliferation of HSCs accompanied by a decrease in the expression of Cyclin D1. The protein level of proliferating cell nuclear antigen was decreased in activated HSCs following a gradient concentration of Sophocarpine. CONCLUSION: Sophocarpine can alleviate liver fibrosis mainly by inhibiting the TLR4 pathway. Sophocarpine may be a potential chemotherapeutic agent for chronic liver diseases.

Sophocarpine and matrine inhibit the production of TNF-alpha and IL-6 in murine macrophages and prevent cachexia-related symptoms induced by colon26 adenocarcinoma in mice.[Pubmed:18775799]

Int Immunopharmacol. 2008 Dec 20;8(13-14):1767-72.

The present study aims to access the effects of sophora alkaloids on the production of pro-inflammatory cytokines and evaluate their therapeutic efficiency on cachexia. The comparative study showed that all sophora alkaloids tested here, including matrine, oxymatrine, Sophocarpine, sophoramine, and sophoridine, inhibited TNF-alpha and IL-6 production in both RAW264.7 cells and murine primary macrophages, and Sophocarpine showed the most potent inhibitory effect among them. Quantification of TNF-alpha and IL-6 mRNA in RAW264.7 cells by real-time RT-PCR revealed that both Sophocarpine and matrine suppressed TNF-alpha and IL-6 expression and Sophocarpine has stronger suppressing potency than matrine. Inoculation (s.c.) of colon26 adenocarcinoma cells into BALB/c mice induced cachexia, as evidenced by progressive weight loss, reduction in food intake, wasting of gastrocnemius muscle and epididymal fat, and increase in serum levels of TNF-alpha and IL-6. Administration of 50 mg/kg/d Sophocarpine or matrine for 5 days from the onset of cachexia did not inhibit the tumor growth but resulted in attenuation of cachexia symptoms. Furthermore, Sophocarpine and matrine decreased the serum levels of TNF-alpha and IL-6, and Sophocarpine showed a better therapeutic effect than matrine. These results suggest that Sophocarpine and matrine exert anti-cachectic effects probably through inhibition of TNF-alpha and IL-6.

Sophocarpine attenuates wear particle-induced implant loosening by inhibiting osteoclastogenesis and bone resorption via suppression of the NF-kappaB signalling pathway in a rat model.[Pubmed:29130485]

Br J Pharmacol. 2018 Mar;175(6):859-876.

BACKGROUND AND PURPOSE: Aseptic prosthesis loosening, caused by wear particles, is one of the most common causes of arthroplasty failure. Extensive and over-activated osteoclast formation and physiological functioning are regarded as the mechanism of prosthesis loosening. Therapeutic modalities based on inhibiting osteoclast formation and bone resorption have been confirmed to be an effective way of preventing aseptic prosthesis loosening. In this study, we have investigated the effects of Sophocarpine (SPC, derived from Sophora flavescens) on preventing implant loosening and further explored the underlying mechanisms. EXPERIMENTAL APPROACH: The effects of SPC in inhibiting osteoclastogenesis and bone resorption were evaluated in osteoclast formation, induced in vitro by the receptor activator of NF-kappaB ligand (RANKL). A rat femoral particle-induced peri-implant osteolysis model was established. Subsequently, micro-CT, histology, mechanical testing and bone turnover were used to assess the effects of SPC in preventing implant loosening. KEY RESULTS: In vitro, we found that SPC suppressed osteoclast formation, bone resorption, F-actin ring formation and osteoclast-associated gene expression by inhibiting NF-kappaB signalling, specifically by targeting IkappaB kinases. Our in vivo study showed that SPC prevented particle-induced prosthesis loosening by inhibiting osteoclast formation, resulting in reduced periprosthetic bone loss, diminished pseudomembrane formation, improved bone-implant contact, reduced bone resorption-related turnover and enhanced stability of implants. Inhibition of NF-kappaB signalling by SPC was confirmed in vivo. CONCLUSION AND IMPLICATIONS: SPC can prevent implant loosening through inhibiting osteoclast formation and bone resorption. Thus, SPC might be a novel therapeutic agent to prevent prosthesis loosening and for osteolytic diseases.

Sophocarpine alleviates hepatocyte steatosis through activating AMPK signaling pathway.[Pubmed:23395669]

Toxicol In Vitro. 2013 Apr;27(3):1065-71.

Sophocarpine, an effective compound derived from foxtail-like sophora herb and seed, has been reported that it can alleviate non-alcoholic steatohepatitis (NASH) in rats and affect adipocytokine synthesis. Meanwhile, adipocytokines could adjust hepatic lipid metabolism through AMPK signaling pathway. In the work presented here, primary hepatocytes were isolated from specific pathogen-free male SD rats and incubated with 200 mumol/L oleic acid for 24h to induce steatotic model, then treated with Sophocarpine for 72 h. Oil red staining was performed to evaluate steatosis, total RNA and protein of primary hepatocytes were extracted for real-time RT-PCR and western blot analysis. A cluster of aberrances were observed in the model group, including hepatocyte steatosis, increased leptin and decreased adiponectin mRNA expressions. While Sophocarpine treatment resulted in: significant improvement of steatosis (>50% decrease), decrease of leptin expression (<0.57-fold) and increase of adiponectin expression (>1.48-fold). Moreover, compared with the model group, Sophocarpine could significantly increase P-AMPKalpha (>5.82-fold), AMPKalpha (>1.29-fold) and ACC (>3.27-fold) protein expressions, and reduce P-ACC (<0.30-fold) and HNF-4alpha (<0.20-fold) protein expression. The mRNA expression of Srebp-1c was downregulated significantly simultaneously (<0.68-fold). We concluded that Sophocarpine could alleviate hepatocyte steatosis and the potential mechanism might be the activated signaling pathway of AMPK.

Sophocarpine attenuates toll-like receptor 4 in steatotic hepatocytes to suppress pro-inflammatory cytokines synthesis.[Pubmed:25089018]

J Gastroenterol Hepatol. 2015 Feb;30(2):405-12.

BACKGROUND AND AIM: Sophocarpine, a tetracyclic quinolizidine alkaloid derived from Sophora alopecuroides L., has been documented that it can suppress pro-inflammatory cytokines synthesis in alleviating nonalcoholic steatohepatitis (NASH) in vivo. Toll-like receptor 4 (TLR4) is a pattern recognition receptor whose activation results in the production of several pro-inflammatory cytokines. It has been reported that TLR4 is upregulated in nonalcoholic fatty liver disease and plays an important role in the pathogenesis of NASH. This study aimed to examine the changes of TLR4 and its signaling pathways in Sophocarpine's anti-inflammatory process on experimental NASH in vitro. METHODS: Primary hepatocytes were isolated, and oleic acid-induced steatosis model was established. Cell Counting Kit-8 assay was used to detect the number of metabolically active mitochondria and viable cells. Immunocytochemistry analysis was applied to evaluating pro-inflammatory cytokines synthesis. Total RNA and protein were extracted for real-time polymerase chain reaction and Western blot detection. RESULTS: Enhanced expression of TLR4 was observed in oleic acid-induced steatotic hepatocytes. Sophocarpine suppressed pro-inflammatory cytokines synthesis and reduced the expression of TLR4 in steatotic hepatocytes. Expression of TLR4 and pro-inflammatory cytokines recovered after Sophocarpine was removed. Moreover, Sophocarpine restrained the activation of nuclear factor-kappaB (NF-kappaB), c-Jun-N-terminal kinase (JNK), and Extracellular regulated protein kinases (ERK) signaling pathways in the anti-inflammatory process. CONCLUSION: Sophocarpine could decrease the expression of TLR4 in steatotic hepatocytes and suppress pro-inflammatory cytokines synthesis. NF-kappaB, JNK, and ERK signaling pathways were important workable downstream pathways.

Sophocarpine Protects Mice from ConA-Induced Hepatitis via Inhibition of the IFN-Gamma/STAT1 Pathway.[Pubmed:28377718]

Front Pharmacol. 2017 Mar 21;8:140.

Sophocarpine is the major pharmacologically active compound of the traditional Chinese herbal medicine Radix Sophorae Subprostratae which has been used in treating hepatitis for years in China. It has been demonstrated that Sophocarpine exerts an activity in immune modulation and significantly decreases the production of inflammatory cytokines. However, the protective effects of Sophocarpine in T cell-dependent immune hepatitis remained unknown. The aim of this study was to determine the protective effects and pharmacological mechanisms of Sophocarpine on Concanavalin A (ConA)-induced hepatitis, an experimental model of T cell-mediated liver injury. BALB/C mice were pretreated with Sophocarpine or Bicyclol for five consecutive days. Thirty minutes after the final administration, the mice were injected with 15 mgkg(-1) of ConA intravenously. The results indicated that pretreatment with Sophocarpine significantly ameliorated liver inflammation and injury as evidenced by both biochemical and histopathological observations. Moreover, in Sophocarpine-pretreated mice, liver messenger RNA expression levels of chemokines and adhesion molecules, such as macrophage inflammatory protein-1alpha, CXC chemokine ligand 10, and Intercellular adhesion molecule-1, were markedly reduced. Further studies revealed that Sophocarpine significantly downregulated the expression of T-bet via inhibition of signal transducers and activators of transcription1 (STAT1) activation and overexpression of suppressor of cytokine signaling1, inhibiting the activation of Th1 cells and the expression of Interferon-gamma (IFN-gamma). Altogether, these results suggest new opportunities to use Sophocarpine in the treatment of T cell-mediated liver disease. In summary, Sophocarpine could attenuate ConA-induced liver injury, and the protective effect of Sophocarpine was associated with its inhibition effect of pro-inflammatory cytokines, chemokines, and the IFN-gamma/STAT1 signaling pathway.

Description

Sophocarpine (monohydrate) is one of the significant alkaloid extracted from the traditional herb medicine Sophora flavescens which has many pharmacological properties such as anti-virus, anti-tumor, anti-inflammatory. Sophocarpine (monohydrate) significantly inhibits the growth of gastric cancer (GC) cells through multiple mechanisms such as induction of autophagy, activation of cell apoptosis and down-regulation of cell survival PI3K/AKT signaling pathway. Sophocarpine (monohydrate) has been demonstrated to have anti-tumor activity in various cancer cells, including hepatocellular carcinoma, prostate cancer and colorectal cancer.

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