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Bruce K. Cassels - One of the best experts on this subject based on the ideXlab platform.
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structure antioxidant activity relationships in Boldine and glaucine a dft study
New Journal of Chemistry, 2021Co-Authors: Alejandro Vasquezespinal, Bruce K. Cassels, Osvaldo Yañez, Edison Osorio, Carlos Areche, Lina María Ruiz, Olimpo Garciabeltran, William TiznadoAbstract:Previous experimental results on the free radical-scavenging properties of Boldine, one of the most potent natural antioxidants, suggested that the benzylic hydrogen, neighboring a nitrogen lone electron pair, might be the key to its protective and antioxidant effect, in contrast to the usually assumed labile phenolic hydrogen atoms. Our computations suggest that both Boldine and glaucine can undergo two successive hydrogen transfers under attack by an oxidizing radical (from C-6a-H and C-7-H). The hydroxyl groups of Boldine could also participate via the HAT mechanism, although to a lesser extent. In the case of quaternary N-methylated derivatives, the sharing of the nitrogen lone pair makes the transfer of the C-6a hydrogen energetically unfeasible, supporting the earlier proposal based on experimental evidence. The hydroxyl groups of Boldine and its derivatives could contribute to antioxidant activity via the sequential proton loss electron transfer mechanism, although this would only be relevant at higher pH values.
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Structure–antioxidant activity relationships in Boldine and glaucine: a DFT study
New Journal of Chemistry, 2021Co-Authors: Alejandro Vásquez-espinal, Bruce K. Cassels, Osvaldo Yañez, Edison Osorio, Carlos Areche, Olimpo García-beltrán, Lina María Ruiz, William TiznadoAbstract:Previous experimental results on the free radical-scavenging properties of Boldine, one of the most potent natural antioxidants, suggested that the benzylic hydrogen, neighboring a nitrogen lone electron pair, might be the key to its protective and antioxidant effect, in contrast to the usually assumed labile phenolic hydrogen atoms. Our computations suggest that both Boldine and glaucine can undergo two successive hydrogen transfers under attack by an oxidizing radical (from C-6a-H and C-7-H). The hydroxyl groups of Boldine could also participate via the HAT mechanism, although to a lesser extent. In the case of quaternary N-methylated derivatives, the sharing of the nitrogen lone pair makes the transfer of the C-6a hydrogen energetically unfeasible, supporting the earlier proposal based on experimental evidence. The hydroxyl groups of Boldine and its derivatives could contribute to antioxidant activity via the sequential proton loss electron transfer mechanism, although this would only be relevant at higher pH values.
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Boldine inhibits the alveolar bone resorption during ligature-induced periodontitis by modulating the Th17/Treg imbalance.
Journal of periodontology, 2020Co-Authors: Emilio A. Cafferata, Gonzalo Fuentes-barros, Sebastián Castro-saavedra, Samanta Melgar-rodríguez, Felipe Alfaro Rivera, Paola Carvajal, Marcela Hernández, Bastián I Cortés, Cristian Cortez, Bruce K. CasselsAbstract:Background During periodontitis, tooth-supporting alveolar bone is resorbed when there is an increased expression of the pro-osteolytic factor termed receptor activator of nuclear factor κB ligand (RANKL), which is responsible for osteoclast differentiation and activation. In periodontitis-affected tissues, the imbalance between T-helper type-17 (Th17) and T-regulatory (Treg) lymphocyte activity favors this RANKL overexpression. In this context, immunotherapeutic strategies aimed at modulating this Th17/Treg imbalance could eventually arrest the RANKL-mediated alveolar bone loss. Boldine has been reported to protect from pathological bone loss during rheumatoid arthritis and osteoporosis, whose pathogenesis is associated with a Th17/Treg imbalance. However, the effect of Boldine on alveolar bone resorption during periodontitis has not been elucidated yet. This study aimed to determine whether Boldine inhibits alveolar bone resorption by modulating the Th17/Treg imbalance during periodontitis. Methods Mice with ligature-induced periodontitis were orally treated with Boldine (10/20/40 mg/kg) for 15 consecutive days. Non-treated periodontitis-affected mice and non-ligated mice were used as controls. Alveolar bone loss was analyzed by micro-computed tomography and scanning electron microscopy. Osteoclasts were quantified by histological identification of tartrate-resistant acid phosphatase-positive cells. Production of RANKL and its competitive antagonist osteoprotegerin (OPG) were analyzed by ELISA, quantitative polymerase chain reaction (qPCR), and immunohistochemistry. The Th17 and Treg responses were analyzed by quantifying the T-cell frequency and number by flow cytometry. Also, the expression of their signature transcription factors and cytokines were quantified by qPCR. Results Boldine inhibited the alveolar bone resorption. Consistently, Boldine caused a decrease in the osteoclast number and RANKL/OPG ratio in periodontal lesions. Besides, Boldine reduced the Th17-lymphocyte detection and response and increased the Treg-lymphocyte detection and response in periodontitis-affected tissues. Conclusion Boldine, administered orally, inhibited the alveolar bone resorption and modulated the Th17/Treg imbalance during experimental periodontitis.
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Telomerase Inhibition by a New Synthetic Derivative of the Aporphine Alkaloid Boldine
International journal of molecular sciences, 2018Co-Authors: Sakineh Kazemi Noureini, Mitra Kheirabadi, Fatima Masoumi, Farve Khosrogerdi, Younes Zarei, Cristian Suárez-rozas, Julio Salas-norambuena, Bruce K. CasselsAbstract:Telomerase, the enzyme responsible for cell immortality, is an important target in anti-cancer drug discovery. Boldine, an abundant aporphine alkaloid of Peumus boldus, is known to inhibit telomerase at non-toxic concentrations. Cytotoxicity of N-benzylsecoBoldine hydrochloride (BSB), a synthetic derivative of Boldine, was determined using the MTT method in MCF7 and MDA-MB231 cells. Aliquots of cell lysates were incubated with various concentrations of BSB in qTRAP (quantitative telomere repeat amplification protocol)-ligand experiments before substrate elongation by telomerase or amplification by hot-start Taq polymerase. The crystal structure of TERT, the catalytic subunit of telomerase from Tribolium castaneum, was used for docking and molecular dynamics analysis. The qTRAP-ligand data gave an IC50 value of about 0.17 ± 0.1 µM for BSB, roughly 400 times stronger than Boldine, while the LD50 in the cytotoxicity assays were 12.5 and 21.88 µM, respectively, in cells treated for 48 h. Although both compounds interacted well with the active site, MD analysis suggests a second binding site with which BSB interacts via two hydrogen bonds, much more strongly than Boldine. Theoretical analyses also evaluated the IC50 for BSB as submicromolar. BSB, with greater hydrophobicity and flexibility than Boldine, represents a promising structure to inhibit telomerase at non-toxic concentrations.
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Variation of the alkaloid content of Peumus boldus (boldo).
Fitoterapia, 2018Co-Authors: Gonzalo Fuentes-barros, Sebastián Castro-saavedra, Leonel Liberona, Williams Acevedo-fuentes, Cristian Tirapegui, César Mattar, Bruce K. CasselsAbstract:Eighteen alkaloids were detected in the bark, leaves, wood and roots of Peumus boldus, including traces of secoBoldine, N-methylsecoBoldine (Boldine methine), glaucine and norreticuline, not reported previously as constituents of this species. Using appropriate standards, we quantified thirteen of them by UHPLC-MS/MS. Boldine was dominant in the bark, and laurolitsine in wood and roots. The alkaloid composition of the leaves, determined for 130 individually identified trees, classified by age and sex, was highly variable, where N-methyllaurotetanine, laurotetanine, coclaurine and in some cases isocorydine predominated, but not Boldine.
Hernan Speisky - One of the best experts on this subject based on the ideXlab platform.
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Biological disposition of Boldine: in vitro and in vivo studies
Phytotherapy research : PTR, 2000Co-Authors: Inés Jiménez, Hernan SpeiskyAbstract:Boldine is a natural compound with well-established free radical scavenger and hepatoprotective properties. The further exploration of its actual therapeutic potential as an antioxidant is, however, partially limited by the absence of knowledge on its pharmacokinetics. In the present studies, we provide information on the in vitro and in vivo biological disposition of Boldine. The addition of 200 microM Boldine to an isolated rat hepatocyte suspension was followed by a time-dependent (0-60 min) disappearance of Boldine from the extracellular medium. This decline was associated with an early (first 2 min) and swift accumulation (1600 microM) of Boldine within the cells. Although the intracellular concentration of Boldine diminished, Boldine was always found to occur within the cells at concentrations substantially higher than those initially added to the preparation. Boldine was also concentration-dependently removed from the extracellular medium by isolated rat livers portally perfused with the antioxidant. In vivo studies, conducted in rats, revealed that following either its oral or its intravenous administration, plasma Boldine concentrations declined rapidly and according to an apparently first order type of kinetics. After its oral administration (50 or 75 mg/kg), Boldine was rapidly (within 30 min) absorbed and preferentially concentrated in the liver, with substantially lower concentrations being found in the brain and heart. Maximal hepatic concentrations of Boldine were found to be equal to or greater than those needed to afford antioxidant and hepatoprotective effects in vitro.
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Protective effects of Boldine against free radical-induced erythrocyte lysis.
Phytotherapy research : PTR, 2000Co-Authors: Inés Jiménez, R. Bannach, Argelia Garrido, Martin Gotteland, Hernan SpeiskyAbstract:Boldine, an aporphine alkaloid extracted from the leaves and bark of boldo (Peumus boldus Mol.), has been shown to exhibit strong free-radical scavenger and antioxidant properties. Here, we report the in vitro ability of Boldine to protect intact red cells against the haemolytic damage induced by the free radical initiator 2,2′-azobis-(2-amidinopropane) (AAPH). Boldine concentration-dependently prevented the AAPH-induced leakage of haemoglobin into the extracellular medium. Substantial and similar cyto-protective effects of Boldine were observed whether the antioxidant was added 1 h prior to, or simultaneously with, the azo-compound. The delayed addition of Boldine, by 1 h relative to AAPH, diminished but did not abolish its cytoprotective effect. However, negligible effects of Boldine were observed after its addition to erythrocytes previously incubated with AAPH for 2 h. The data presented demonstrate that, in addition to its well-established antioxidant effects, Boldine also displays time-dependently strong cytoprotective properties against chemically induced haemolytic damage. Copyright © 2000 John Wiley & Sons, Ltd.
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biochemical and behavioral effects of Boldine and glaucine on dopamine systems
Pharmacology Biochemistry and Behavior, 1999Co-Authors: Marcelo Asencio, B Delaquerriere, Etienne Comoy, Bruce K. Cassels, Hernan Speisky, Philippe ProtaisAbstract:Abstract The aporphine alkaloids Boldine and glaucine have been reported to show “neuroleptic-like” actions in mice, suggesting that they may act as dopamine antagonists. We have found that in vitro Boldine displaces specific striatal [ 3 H]-SCH 23390 binding with IC 50 = 0.4 μM and [ 3 H]-raclopride binding with IC 50 = 0.5 μM, while the affinities of glaucine at the same sites are an order of magnitude lower. In vivo, however, 40 mg/kg Boldine (IP) did not modify specific striatal [ 3 H]-raclopride binding and only decreased [ 3 H]-SCH 23390 binding by 25%. On the other hand, 40 mg/kg glaucine (IP) displaced both radioligands by about 50%. Behaviors (climbing, sniffing, grooming) elicited in mice by apomorphine (0.75 mg/kg SC) were not modified by Boldine at doses up to 40 mg/kg (IP) but were almost completely abolished by 40 mg/kg glaucine (IP). In the apomorphine-induced (0.1 mg/kg SC) rat yawning and penile erection model, Boldine and glaucine appeared to be similarly effective, inhibiting both behaviors by more than 50% at 40 mg/kg (IP). Boldine and glaucine, injected IP at doses up to 40 mg/kg, were poor modifiers of dopamine metabolism in mouse and rat striatum. These data suggest that Boldine does not display effective central dopaminergic antagonist activities in vivo in spite of its good binding affinity at D 1 - and D 2 -like receptors, and that glaucine, although less effective in vitro, does appear to exhibit some antidopaminergic properties in vivo.
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Protective effect of Boldine in experimental colitis.
Planta medica, 1997Co-Authors: Martin Gotteland, Bruce K. Cassels, Inés Jiménez, Oscar Brunser, Leda Guzman, Sergio Romero, Hernan SpeiskyAbstract:The cytoprotective and anti-inflammatory effects of Boldine in an experimental model of acute colitis are reported. The administration of Boldine to animals with colitis induced by the intrarectal administration of acetic acid, was found to protect against colonic damage as expressed by major reductions in the extent of cell death, tissue disorganization, and edema. Boldine also reduced the colonic neutrophil infiltration, as measured by the myeloperoxidase activity, but it did not significantly affect tissue lipoperoxides. Boldine was found to preserve the colonic fluid transport, a function otherwise markedly affected in the tissue of acid-treated animals. Results presented here provide experimental evidence supporting new cytoprotective and anti-inflammatory properties of Boldine.
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Cytoprotective and antioxidant effects of Boldine on tert-butyl hydroperoxide—induced damage to isolated hepatocytes
Cell Biology and Toxicology, 1996Co-Authors: R. Bannach, Bruce K. Cassels, A. Valenzuela, L. J. Núnez-vergara, Hernan SpeiskyAbstract:Boldine, an aporphine alkaloid, was recently shown by us to exhibit potent antioxidant properties. We report here that Boldine concentration-dependently inhibited the peroxidative (accumulation of thiobarbituric acid reactive substances) and lytic damage (trypan blue exclusion and lactate dehydrogenase leakage) to isolated rat hepatocytes induced by tert -butyl hydroperoxide (TBOOH). Boldine (200 μmol/L) fully cytoprotected and completely prevented the peroxidation induced by TBOOH a concentrations equal to or lower than 0.87 mmol/L. However, at a peroxide concentration of 0.91 mmol/L, although Boldine completely inhibited lipid peroxidation it largely failed to afford cytoprotection against TBOOH. TBOOH alone (0.83 mmol/L) caused an early (within 60 s) sudden decline of reduced glutathione (by 50%) and an equivalent increase in the levels of oxidized glutathione. Neither of these effects was prevented by the simultaneous addition of a cytoprotective and antioxidant concentration of Boldine (200 μmol/L). The delayed addition of Boldine to the suspension (after 10 or 20 min), while effectively blocking any further increase in thiobarbituric acid reactive substances, totally failed to prevent the peroxide-induced loss in cell viability. Conversely, preincubation of the hepatocytes with Boldine for 150 min (at which time no Boldine could be detected in either intra- or extracellular spaces) prevented lipid peroxidation and was as effective in protecting the cells against the damage caused by the subsequent addition of TBOOH as the simultaneous addition of Boldine and TBOOH to hepatocytes preincubated for 150 min under control conditions.
Emilio A. Cafferata - One of the best experts on this subject based on the ideXlab platform.
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Boldine inhibits the alveolar bone resorption during ligature induced periodontitis by modulating the th17 treg imbalance
Journal of Periodontology, 2021Co-Authors: Emilio A. Cafferata, Paola Carvajal, Marcela Hernández, Bastián I Cortés, Sebastian Castrosaavedra, Gonzalo Fuentesbarros, Samanta Melgarrodriguez, Felipe Rivera, Cristian CortezAbstract:Background During periodontitis, tooth-supporting alveolar bone is resorbed when there is an increased expression of the pro-osteolytic factor termed receptor activator of nuclear factor κB ligand (RANKL), which is responsible for osteoclast differentiation and activation. In periodontitis-affected tissues, the imbalance between T-helper type-17 (Th17) and T-regulatory (Treg) lymphocyte activity favors this RANKL overexpression. In this context, immunotherapeutic strategies aimed at modulating this Th17/Treg imbalance could eventually arrest the RANKL-mediated alveolar bone loss. Boldine has been reported to protect from pathological bone loss during rheumatoid arthritis and osteoporosis, whose pathogenesis is associated with a Th17/Treg imbalance. However, the effect of Boldine on alveolar bone resorption during periodontitis has not been elucidated yet. This study aimed to determine whether Boldine inhibits alveolar bone resorption by modulating the Th17/Treg imbalance during periodontitis. Methods Mice with ligature-induced periodontitis were orally treated with Boldine (10/20/40 mg/kg) for 15 consecutive days. Non-treated periodontitis-affected mice and non-ligated mice were used as controls. Alveolar bone loss was analyzed by micro-computed tomography and scanning electron microscopy. Osteoclasts were quantified by histological identification of tartrate-resistant acid phosphatase-positive cells. Production of RANKL and its competitive antagonist osteoprotegerin (OPG) were analyzed by ELISA, quantitative polymerase chain reaction (qPCR), and immunohistochemistry. The Th17 and Treg responses were analyzed by quantifying the T-cell frequency and number by flow cytometry. Also, the expression of their signature transcription factors and cytokines were quantified by qPCR. Results Boldine inhibited the alveolar bone resorption. Consistently, Boldine caused a decrease in the osteoclast number and RANKL/OPG ratio in periodontal lesions. Besides, Boldine reduced the Th17-lymphocyte detection and response and increased the Treg-lymphocyte detection and response in periodontitis-affected tissues. Conclusion Boldine, administered orally, inhibited the alveolar bone resorption and modulated the Th17/Treg imbalance during experimental periodontitis.
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Boldine inhibits the alveolar bone resorption during ligature-induced periodontitis by modulating the Th17/Treg imbalance.
Journal of periodontology, 2020Co-Authors: Emilio A. Cafferata, Gonzalo Fuentes-barros, Sebastián Castro-saavedra, Samanta Melgar-rodríguez, Felipe Alfaro Rivera, Paola Carvajal, Marcela Hernández, Bastián I Cortés, Cristian Cortez, Bruce K. CasselsAbstract:Background During periodontitis, tooth-supporting alveolar bone is resorbed when there is an increased expression of the pro-osteolytic factor termed receptor activator of nuclear factor κB ligand (RANKL), which is responsible for osteoclast differentiation and activation. In periodontitis-affected tissues, the imbalance between T-helper type-17 (Th17) and T-regulatory (Treg) lymphocyte activity favors this RANKL overexpression. In this context, immunotherapeutic strategies aimed at modulating this Th17/Treg imbalance could eventually arrest the RANKL-mediated alveolar bone loss. Boldine has been reported to protect from pathological bone loss during rheumatoid arthritis and osteoporosis, whose pathogenesis is associated with a Th17/Treg imbalance. However, the effect of Boldine on alveolar bone resorption during periodontitis has not been elucidated yet. This study aimed to determine whether Boldine inhibits alveolar bone resorption by modulating the Th17/Treg imbalance during periodontitis. Methods Mice with ligature-induced periodontitis were orally treated with Boldine (10/20/40 mg/kg) for 15 consecutive days. Non-treated periodontitis-affected mice and non-ligated mice were used as controls. Alveolar bone loss was analyzed by micro-computed tomography and scanning electron microscopy. Osteoclasts were quantified by histological identification of tartrate-resistant acid phosphatase-positive cells. Production of RANKL and its competitive antagonist osteoprotegerin (OPG) were analyzed by ELISA, quantitative polymerase chain reaction (qPCR), and immunohistochemistry. The Th17 and Treg responses were analyzed by quantifying the T-cell frequency and number by flow cytometry. Also, the expression of their signature transcription factors and cytokines were quantified by qPCR. Results Boldine inhibited the alveolar bone resorption. Consistently, Boldine caused a decrease in the osteoclast number and RANKL/OPG ratio in periodontal lesions. Besides, Boldine reduced the Th17-lymphocyte detection and response and increased the Treg-lymphocyte detection and response in periodontitis-affected tissues. Conclusion Boldine, administered orally, inhibited the alveolar bone resorption and modulated the Th17/Treg imbalance during experimental periodontitis.
Alberto Navalón - One of the best experts on this subject based on the ideXlab platform.
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Determination of Boldine in drug formulations by first-derivative synchronous spectrofluorimetry
Journal of pharmaceutical and biomedical analysis, 1994Co-Authors: José Luis Vilchez, Gonzalo Sánchez-palencia, Ramiro Avidad, Alberto NavalónAbstract:Abstract A simple and sensitive method is proposed for the determination of Boldine by first-derivative synchronous spectrofluorimetry based on its native fluorescence in 0.1 N sulphuric acid. The constant wavelength difference ( Δλ = λ cm - λ c chosen to optimize the determination is 90 nm. The linear concentration range of application is between 2.0 and 50.0 wg I- −1 of Boldine. the detection limit 0.4 wg l −1 and the relative standard deviation at a concentration of 25 μg l −1 was 2.19%. The method has been satisfactorily applied to the determination of Boldine in pharmaceutical formulations.
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Simultaneous determination of yohimbine and Boldine by first-derivative synchronous spectrofluorimetry
Microchimica Acta, 1993Co-Authors: José Luis Vilchez, Gonzalo Sánchez-palencia, Ramiro Avidad, Luis Fermín Capitán-vallvey, Alberto NavalónAbstract:A method for the simultaneous determination of yohimbine and Boldine in mixtures by first-derivative synchronous spectrofluorimetry has been developed. The method is based on their native fluorescence in 0.1 N sulphuric acid medium. The constant wavelength difference chosen to optimize the determination was Δλ=λ_em -λ_em=82 nm. Yohimbine was measured at λ_ex//λ_em= 285/367 nm, and Boldine at λ_ex/λ_em=272/354 nm. The range of application is 10–500 μg/l for yohimbine and 1–50 μg/l for Boldine. The method was applied to the determination of yohimbine and Boldine in synthetic mixtures and pharmaceuticals, with errors generally ⩽2%. Relative standard deviations were about 2%.
Cristian Cortez - One of the best experts on this subject based on the ideXlab platform.
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Boldine inhibits the alveolar bone resorption during ligature induced periodontitis by modulating the th17 treg imbalance
Journal of Periodontology, 2021Co-Authors: Emilio A. Cafferata, Paola Carvajal, Marcela Hernández, Bastián I Cortés, Sebastian Castrosaavedra, Gonzalo Fuentesbarros, Samanta Melgarrodriguez, Felipe Rivera, Cristian CortezAbstract:Background During periodontitis, tooth-supporting alveolar bone is resorbed when there is an increased expression of the pro-osteolytic factor termed receptor activator of nuclear factor κB ligand (RANKL), which is responsible for osteoclast differentiation and activation. In periodontitis-affected tissues, the imbalance between T-helper type-17 (Th17) and T-regulatory (Treg) lymphocyte activity favors this RANKL overexpression. In this context, immunotherapeutic strategies aimed at modulating this Th17/Treg imbalance could eventually arrest the RANKL-mediated alveolar bone loss. Boldine has been reported to protect from pathological bone loss during rheumatoid arthritis and osteoporosis, whose pathogenesis is associated with a Th17/Treg imbalance. However, the effect of Boldine on alveolar bone resorption during periodontitis has not been elucidated yet. This study aimed to determine whether Boldine inhibits alveolar bone resorption by modulating the Th17/Treg imbalance during periodontitis. Methods Mice with ligature-induced periodontitis were orally treated with Boldine (10/20/40 mg/kg) for 15 consecutive days. Non-treated periodontitis-affected mice and non-ligated mice were used as controls. Alveolar bone loss was analyzed by micro-computed tomography and scanning electron microscopy. Osteoclasts were quantified by histological identification of tartrate-resistant acid phosphatase-positive cells. Production of RANKL and its competitive antagonist osteoprotegerin (OPG) were analyzed by ELISA, quantitative polymerase chain reaction (qPCR), and immunohistochemistry. The Th17 and Treg responses were analyzed by quantifying the T-cell frequency and number by flow cytometry. Also, the expression of their signature transcription factors and cytokines were quantified by qPCR. Results Boldine inhibited the alveolar bone resorption. Consistently, Boldine caused a decrease in the osteoclast number and RANKL/OPG ratio in periodontal lesions. Besides, Boldine reduced the Th17-lymphocyte detection and response and increased the Treg-lymphocyte detection and response in periodontitis-affected tissues. Conclusion Boldine, administered orally, inhibited the alveolar bone resorption and modulated the Th17/Treg imbalance during experimental periodontitis.
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Boldine inhibits the alveolar bone resorption during ligature-induced periodontitis by modulating the Th17/Treg imbalance.
Journal of periodontology, 2020Co-Authors: Emilio A. Cafferata, Gonzalo Fuentes-barros, Sebastián Castro-saavedra, Samanta Melgar-rodríguez, Felipe Alfaro Rivera, Paola Carvajal, Marcela Hernández, Bastián I Cortés, Cristian Cortez, Bruce K. CasselsAbstract:Background During periodontitis, tooth-supporting alveolar bone is resorbed when there is an increased expression of the pro-osteolytic factor termed receptor activator of nuclear factor κB ligand (RANKL), which is responsible for osteoclast differentiation and activation. In periodontitis-affected tissues, the imbalance between T-helper type-17 (Th17) and T-regulatory (Treg) lymphocyte activity favors this RANKL overexpression. In this context, immunotherapeutic strategies aimed at modulating this Th17/Treg imbalance could eventually arrest the RANKL-mediated alveolar bone loss. Boldine has been reported to protect from pathological bone loss during rheumatoid arthritis and osteoporosis, whose pathogenesis is associated with a Th17/Treg imbalance. However, the effect of Boldine on alveolar bone resorption during periodontitis has not been elucidated yet. This study aimed to determine whether Boldine inhibits alveolar bone resorption by modulating the Th17/Treg imbalance during periodontitis. Methods Mice with ligature-induced periodontitis were orally treated with Boldine (10/20/40 mg/kg) for 15 consecutive days. Non-treated periodontitis-affected mice and non-ligated mice were used as controls. Alveolar bone loss was analyzed by micro-computed tomography and scanning electron microscopy. Osteoclasts were quantified by histological identification of tartrate-resistant acid phosphatase-positive cells. Production of RANKL and its competitive antagonist osteoprotegerin (OPG) were analyzed by ELISA, quantitative polymerase chain reaction (qPCR), and immunohistochemistry. The Th17 and Treg responses were analyzed by quantifying the T-cell frequency and number by flow cytometry. Also, the expression of their signature transcription factors and cytokines were quantified by qPCR. Results Boldine inhibited the alveolar bone resorption. Consistently, Boldine caused a decrease in the osteoclast number and RANKL/OPG ratio in periodontal lesions. Besides, Boldine reduced the Th17-lymphocyte detection and response and increased the Treg-lymphocyte detection and response in periodontitis-affected tissues. Conclusion Boldine, administered orally, inhibited the alveolar bone resorption and modulated the Th17/Treg imbalance during experimental periodontitis.