BACKGROUND:Relatively or absolutely active bone resorption function of osteoclasts is one of the causative factors of osteoporosis. Therefore,how to inhibit the formation of osteoclasts and reduce the bone resorption activity is a key element in the prevention and treatment of osteoporosis. Liquiritin,which is derived from licorice,plays a role in the clinical treatment of bone diseases,but there are fewer studies addressing the application of liquiritin in osteoporosis and the mechanism is unknown.OBJECTIVE:To confirm,through both in vivo and in vitro experiments,that liquiritin inhibits osteoclast differentiation and alleviates bone loss.METHODS:Cell counting kit-8 was used to detect whether Liquiritin exerts toxic or proliferative effects on mouse bone marrow-derived macrophages,and tartrate-resistant acid phosphatase staining was performed to observe the effect of liquiritin in inhibiting osteoclast differentiation. The affinity of liquiritin binding to proteins related to osteoclast differentiation was verified by network pharmacology. RT-PCR and western blot assays were performed to detect the inhibitory effects of liquiritin on osteoclast-specific protein and gene expression as well as relevant signaling pathways. Finally,the mitigating effect of liquiritin on bone loss was verified in the C57BL/6J mouse osteoporosis model.RESULTS AND CONCLUSION:Liquiritin,at concentrations of 20 μmol/L and below,could inhibit the formation and differentiation of osteoclasts. Concurrently,it exhibited a high affinity with osteoclast-specific proteins such as nuclear factor of activated T-cells 1,Cathepsin K,c-Fos,and matrix metalloproteinase 9,and reduced the relative expression levels of these genes and proteins. Liquiritin could also effectively lower the phosphorylation expression level of JNK in the MAPK signaling pathway at the 15th,30th,45th,and 60th minutes,and it could salvage the degradation of nuclear factor-κB inhibitor α in the nuclear factor-κB signaling pathway at the 60th minute. In vivo experiments demonstrated that liquiritin could mitigate bone loss caused by osteoclasts and improve parameters related to trabecular bone. To conclude,liquiritin possesses the capacity to inhibit osteoclast differentiation and alleviate bone loss,thereby exerting a protective role against osteoporosis.

BACKGROUND:Relatively or absolutely active bone resorption function of osteoclasts is one of the causative factors of osteoporosis. Therefore,how to inhibit the formation of osteoclasts and reduce the bone resorption activity is a key element in the prevention and treatment of osteoporosis. Liquiritin,which is derived from licorice,plays a role in the clinical treatment of bone diseases,but there are fewer studies addressing the application of liquiritin in osteoporosis and the mechanism is unknown.OBJECTIVE:To confirm,through both in vivo and in vitro experiments,that liquiritin inhibits osteoclast differentiation and alleviates bone loss.METHODS:Cell counting kit-8 was used to detect whether Liquiritin exerts toxic or proliferative effects on mouse bone marrow-derived macrophages,and tartrate-resistant acid phosphatase staining was performed to observe the effect of liquiritin in inhibiting osteoclast differentiation. The affinity of liquiritin binding to proteins related to osteoclast differentiation was verified by network pharmacology. RT-PCR and western blot assays were performed to detect the inhibitory effects of liquiritin on osteoclast-specific protein and gene expression as well as relevant signaling pathways. Finally,the mitigating effect of liquiritin on bone loss was verified in the C57BL/6J mouse osteoporosis model.RESULTS AND CONCLUSION:Liquiritin,at concentrations of 20 μmol/L and below,could inhibit the formation and differentiation of osteoclasts. Concurrently,it exhibited a high affinity with osteoclast-specific proteins such as nuclear factor of activated T-cells 1,Cathepsin K,c-Fos,and matrix metalloproteinase 9,and reduced the relative expression levels of these genes and proteins. Liquiritin could also effectively lower the phosphorylation expression level of JNK in the MAPK signaling pathway at the 15th,30th,45th,and 60th minutes,and it could salvage the degradation of nuclear factor-κB inhibitor α in the nuclear factor-κB signaling pathway at the 60th minute. In vivo experiments demonstrated that liquiritin could mitigate bone loss caused by osteoclasts and improve parameters related to trabecular bone. To conclude,liquiritin possesses the capacity to inhibit osteoclast differentiation and alleviate bone loss,thereby exerting a protective role against osteoporosis.

In mating of Lentinula edodes, dikaryotic strains generated from certain monokaryotic strains such as the B2 used in this study tend to show better quality of fruiting bodies regardless of the mated monokaryotic strains. Unlike B2, dikaryotic strains generated from B16 generally show low yields, with deformed or underdeveloped fruiting bodies. This indicates that the two nuclei in the cytoplasm do not contribute equally to the physiology of dikaryotic L. edodes, suggesting an expression bias in the allelic genes of the two nuclei. To understand the role of each nucleus in dikaryotic strains, we investigated single nucleotide polymorphisms (SNPs) in laccase genes of monokaryotic strains to reveal nuclear origin of the expressed mRNAs in dikaryotic strain. We performed reverse transcription PCR (RT-PCR) analysis using total RNAs extracted from dikaryotic strains (A5B2, A18B2, and A2B16) as well as from compatible monokaryotic strains (A5, A18, and B2 for A5B2 and A18B2; A2 and B16 for A2B16). RT-PCR results revealed that Lcc1, Lcc2, Lcc4, Lcc7, and Lcc10 were the mainly expressed laccase genes in the L. edodes genome. To determine the nuclear origin of these laccase genes, the genomic DNA sequences in monokaryotic strains were analyzed, thereby revealing five SNPs in Lcc4 and two in Lcc7. Subsequent sequence analysis of laccase mRNAs expressed in dikaryotic strains revealed that these were almost exclusively expressed from B2-originated nuclei in A5B2 and A18B2 whereas B16 nucleus did not contribute to laccase expression in A2B16 strain. This suggests that B2 nucleus dominates the expression of allelic genes, thereby governing the physiology of dikaryons.
Base Sequence ; Bias (Epidemiology) ; Cytoplasm ; Fruit ; Genome ; Laccase* ; Lentinula* ; Physiology ; Polymerase Chain Reaction ; Polymorphism, Single Nucleotide ; Reverse Transcription ; RNA ; RNA, Messenger ; Sequence Analysis ; Shiitake Mushrooms*

Objective Kidney-supplementing and blood-activating method was adopted in treating senile patients with isolated systolic hypertension to observe its decompression effects and influences on microalbunminuria (Malb),retinol binding protein (RBP) level in 24 hours.Methods 90 patients with simple systolic hypertension were randomly recurited into two groups.52 cases in the treatment group were administered with kidney-supplementing and blood-activating decoction,including 1 case falling off and 51 cases entering statistical analysis; 38 cases in the control group were administered with oral placebo,among them 2 cases were fallen offand 36 cases were entered statistical analysis.Both groups were treated for 8 weeks.Results () Blood pressure:systolic blood pressure at 4 and 8 weeks after the treatment in the treatment group [(144.03±12.33)mmHg (1 mmHg=0.133kPa) and (132.27±13.15)mmHg] wassignificantlyimproved than before the treatment [(156.32±12.05)mm Hg] (P＜0.05),and also significantly better than the control group at 4,8 weeks after the treatment [(151.19± 13.83)mm Hg,(152.74± 12.03)mm Hg] (P＜0.05).②The Malb,RBP level:Malb,RBP level [(40.80±13.51)mg/L,(150.43±23.62)mg/L] after the treatment in the treatment group was reduced than before the treatment [(50.14± 15.61)mg/L,(220.04±30.20) mg/L] (P＜0.05),and was significantly different to the control group after treatment [(52.12±14.69)mg/L,(219.34±34.37)mg/L] (P＜0.05).Conclusion Kidney-supplementing and blood-activating method can improve kidney function,and thus to reduce the effect of systolic blood pressure.

AIM: To observe the heart rate、 electrocardiogram and electrophysiology effect of Qibo Capsule (Radix astragali, Radix aconii lateralis praeparata, etc) on rabbit model with sick sinus syndrome (SND), and to explore their therapy and mechanism. METHODS: 30 rabbits were used to establish sick sinus syndrome models and divided randomly into 3 groups: model group、 Qibo Capsule group、 Xinbao Pill group. To observe the changes of heart rate、 electrocardiogram、electrophysiology after 10 d. RESULTS: Comparison with the model group, the Qibo Capsule group had significant statistics differences in SCL (sinus cardiac cycle)、 SACT (sinoartrial conduction time)、 SNRT (sinus node recovery time)、 SNRTc (corrected sinus node recover time) and HR (heart rate) item (P0.05). CONCLUSION : The experiments show that Qibo Capsule is effective in the recovery of the functional harm of SND rabbits. It is worth further studys.