关键词：
biochemical parameters;diabetes mellitus;glycation;medicinal plants;Wistar rat
摘要：
Different allopathic drugs are being used for the treatment of diabetes mellitus but more emphasis are being placed on the use of medicinal plants, herbs, and natural extracts of fruits and vegetables due to their easy availability, easy consummation with low cost, and with no well-reported side effects. White skinned sweet potato (WSSP; Ipomoea batatas L.) peel-off was selected to find out its antidiabetic potential as well as to explore the effects on selected biochemical parameters in diabetes-induced Wistar rats. In young (3–4 months) and old (up to 1 year) diabetic Wistar rats, it was found that WSSP (I. batatas L.) peel-off significantly (P < 0.05) decreased blood glucose level, protein glycation level, total cholesterol, triglycerides, and low-density lipoprotein (LDL)-cholesterol. A significant (P < 0.05) increase in high-density lipoprotein (HDL)-cholesterol level after treatment was also reported. Furthermore, it was also found that WSSP peel-off also had beneficial effects on total protein concentration, albumin, globulin, and liver enzymes (serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT)). It might be concluded that antidiabetic potential of WSSP extract is due to the presence of bioactive compounds like glycoprotein, anthocyanins, alkaloids, and flavonoids, which act as insulin-like molecules or insulin secretagogues constituents in sweet potatoes peel-off and these antidiabetic proteins were extracted out in more concentration in methanol due to its organic nature. Further research is needed to purify and quantify the antidiabetic components responsible for antidiabetic effects of WSSP and it should be available in compact dose form for the treatment of diabetic patients.
摘要：
Major depressive disorder (MDD) is a chronic and debilitating illness that affects over 350 million people worldwide; however, current treatments have failed to cure or prevent the progress of depression. Increasing evidence suggests a crucial role for connexins in MDD. In this review, we have summarised recent accomplishments regarding the role of connexins, gap junctions, and hemichannels in the aetiology of MDD, and discussed the limitations of current research. A blockage of gap junctions or hemichannels induces depressive behaviour. Possible underlying mechanisms include the regulation of neurosecretory functions and synaptic activity by gap junctions and hemichannels. Gap junctions are functionally inhibited under stress conditions. Conversely, hemichannel permeability is increased. Antidepressants inhibit hemichannel permeability; however, they have contrasting effects on the function of gap junctions under normal conditions and can protect them against stress. In conclusion, the blockage of hemichannels concurrent with improvements in gap junction functionality might be potential targets for depression treatment. (C) 2018 Elsevier B.V. and ECNP. All rights reserved.
摘要：
Myelin is a membrane wrapped around the axon of the nerve cell, which is composed of the mature oligodendrocytes. The role of myelin is to insulate and prevent the nerve electrical impulses from the axon of the neurons to the axons of the other neurons, which is essential for the proper functioning of the nervous system. Minor changes in myelin thickness could lead to substantial changes in conduction speed and may thus alter neural circuit function. Demyelination is the myelin damage, which characterized by the loss of nerve sheath and the relative fatigue of the neuronal sheath and axon. Studies have shown that myelin injury may be closely related to neurodegenerative diseases and may be an early diagnostic criteria and therapeutic target. Thus this review summarizes the recent result of pathologic effect and signal pathways of myelin injury in neurodegenerative diseases, especially the Alzheimer's disease to provide new and effective therapeutic targets.
期刊：
Journal of Microbiology,2018年56(11):805-812 ISSN：1225-8873
通讯作者：
Zhan, Jixun;Wang, Wei
作者机构：
[Xu, Fuchao; Yan, Huiwen; Yan, Riming; Qiu, Yixing; Sun, Lei; Huang, Jinge; Zhan, Jixun] Utah State Univ, Dept Biol Engn, Logan, UT 84322 USA.;[Yan, Huiwen] Cent S Univ, State Key Lab Med Genet, Changsha 410083, Hunan, Peoples R China.;[Yan, Huiwen] Cent S Univ, Sch Life Sci, Changsha 410083, Hunan, Peoples R China.;[Wang, Wei; Zhan, Jixun; Qiu, Yixing] Hunan Univ Chinese Med, TCM, Changsha 410208, Hunan, Peoples R China.;[Wang, Wei; Zhan, Jixun; Qiu, Yixing] Hunan Univ Chinese Med, Ethnomed Innovat & Dev Lab, Sch Pharm, Changsha 410208, Hunan, Peoples R China.
通讯机构：
[Zhan, Jixun] U;[Wang, W; Zhan, JX] H;Utah State Univ, Dept Biol Engn, Logan, UT 84322 USA.;Hunan Univ Chinese Med, TCM, Changsha 410208, Hunan, Peoples R China.;Hunan Univ Chinese Med, Ethnomed Innovat & Dev Lab, Sch Pharm, Changsha 410208, Hunan, Peoples R China.
关键词：
Shiraia sp. Slf14;alk(en)ylresorcinols;precursor-directed biosynthesis;substrate flexibility;type III polyketide synthase
摘要：
A new type III polyketide synthase gene (Ssars) was discovered from the genome of Shiraia sp. Slf14, an endophytic fungal strain from Huperzia serrata. The intron-free gene was cloned from the cDNA and ligated to two expression vectors pET28a and YEpADH2p-URA3 for expression in Escherichia coli BL21(DE3) and Saccharomyces cerevisiae BJ5464, respectively. SsARS was efficiently expressed in E. coli BL21(DE3), leading to the synthesis of a series of polyketide products. Six major products were isolated from the engineered E. coli and characterized as 1,3-dihydroxyphenyl-5-undecane, 1,3-dihydroxyphenyl-5-cis-6′-tridecene,1,3-dihydroxyphenyl-5-tridecane, 1,3-dihydroxyphenyl-5-cis-8′-pentadecene, 1,3-dihydroxyphenyl-5-pentadecane, and 1,3-dihydroxyphenyl-5-cis-10′-heptadecene, respectively, based on the spectral data and biosynthetic origin. Expression of SsARS in the yeast also led to the synthesis of the same polyketide products, indicating that this enzyme can be reconstituted in both heterologous hosts. Supplementation of soybean oil into the culture of E. coli BL21(DE3)/SsARS increased the production titers of 1–6 and led to the synthesis of an additional product, which was identified as 5-(8′Z,11′Z-heptadecadienyl) resorcinol. This work thus allowed the identification of SsARS as a 5-alk(en)ylresorcinol synthase with flexible substrate specificity toward endogenous and exogenous fatty acids. Desired resorcinol derivatives may be synthesized by supplying corresponding fatty acids into the culture medium.
关键词：
Axl inhibitors;Receptor tyrosine kinase;Cancer;Targeted therapy;Small chemicals
摘要：
Overexpression and activation of Axl receptor tyrosine kinase have been widely accepted to promote cell proliferation, chemotherapy resistance, invasion, and metastasis in several human cancers, such as lung, breast, and pancreatic cancers. Axl, a member of the TAM (Tyro3, Axl, Mer) family, and its inhibitors can specifically break the kinase signaling nodes, allowing advanced patients to regain drug sensitivity with improved therapeutic efficacy. Therefore, the research on Axl is promising and it is worthy of further investigations. In this review, we present an update on the Axl inhibitors and provide new insights into their latent application.
作者机构：
[Wang, Zhen-Zhen; Lou, Yu-Xia; Gao, Yan; Chen, Nai-Hong; Xia, Cong-Yuan; Chen, Jiao; Ren, Qian; Zhang, Zhao; Du, Guo-Hua] Chinese Acad Med Sci, State Key Lab Bioact Subst & Funct Nat Med, Inst Mat Med, Beijing 100050, Peoples R China.;[Wang, Zhen-Zhen; Lou, Yu-Xia; Gao, Yan; Chen, Nai-Hong; Xia, Cong-Yuan; Chen, Jiao; Ren, Qian; Zhang, Zhao; Du, Guo-Hua] Chinese Acad Med Sci, Neurosci Ctr, Beijing 100050, Peoples R China.;[Wang, Zhen-Zhen; Lou, Yu-Xia; Gao, Yan; Chen, Nai-Hong; Xia, Cong-Yuan; Chen, Jiao; Ren, Qian; Zhang, Zhao; Du, Guo-Hua] Peking Union Med Coll, Beijing 100050, Peoples R China.;[Chen, Nai-Hong; Wang, Ying-Ying] Guangzhou Univ Chinese Med, Guangzhou 510000, Guangdong, Peoples R China.;[Chen, Nai-Hong; Luo, Piao] Hunan Univ Chinese Med, Coll Pharm, Changsha 410208, Hunan, Peoples R China.
通讯机构：
[Chen, Nai-Hong] C;[Chen, Nai-Hong] P;Chinese Acad Med Sci, State Key Lab Bioact Subst & Funct Nat Med, Inst Mat Med, Beijing 100050, Peoples R China.;Chinese Acad Med Sci, Neurosci Ctr, Beijing 100050, Peoples R China.;Peking Union Med Coll, Beijing 100050, Peoples R China.
摘要：
Increasing evidence has implicated astrocyte pathology in the etiopathology of major depressive disorder (MDD). In particular, dysfunction of gap junctions in astrocytes is a potential target for MDD treatment. However, the mechanism underlying stress-induced dysfunction of gap junctions is still unknown. We therefore studied the mechanism of stress-induced dysfunction of gap junctions in prefrontal cortical and hippocampal astrocytes. Corticosterone (CORT) was used to induce stress conditions; CORT damaged the function of gap junctions, which resulted from less distribution of connexin43 (Cx43) on membranes and the enhanced phosphorylation of Cx43 at 5368. Moreover, CORT downregulated the biosynthesis of Cx43 but increased the degradation of Cx43. Interestingly, both autophagy and the proteasome system were involved in the degradation of Cx43 in prefrontal cortical astrocytes, but only the proteasome system was involved in the degradation of Cx43 in hippocampal astrocytes. CORT significantly induced the formation of annular gap junction vesicles in prefrontal cortical astrocytes; however, Cx43 mainly presented as small dots in the hippocampal astrocytes. Furthermore, CORT increased N-Cadherin expression and the interactions of Cx43 with ZO-1/idrebrin in prefrontal cortical astrocytes, but these interactions were oppositely modulated in hippocampal astrocytes. In conclusion, this study clarified the alternations of the Cx43 life cycle in the prefrontal cortical and hippocampal astrocytes exposed to CORT, which may contribute to our understanding of the mechanisms underlying stress-induced dysfunction of gap junctions. (C) 2017 Elsevier Ltd. All rights reserved.
期刊：
British Journal of Pharmacology,2018年175(4):590-605 ISSN：0007-1188
通讯作者：
Chen, Nai-Hong
作者机构：
[Yang, Peng-Fei; Gao, Yan; Chen, Nai-Hong; Zhang, Zhao; Wang, Sha-Sha; Chu, Shi-Feng] Peking Union Med Coll, Beijing 100050, Peoples R China.;[Yang, Peng-Fei; Gao, Yan; Chen, Nai-Hong; Zhang, Zhao; Wang, Sha-Sha; Chu, Shi-Feng] Chinese Acad Med Sci, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, Beijing, Peoples R China.;[Yang, Peng-Fei; Gao, Yan; Chen, Nai-Hong; Zhang, Zhao; Wang, Sha-Sha; Chu, Shi-Feng] Chinese Acad Med Sci, Neurosci Ctr, Beijing, Peoples R China.;[Ai, Qi-Di; Chen, Nai-Hong; Jiang, Yi-Na] Hunan Univ Chinese Med, Coll Pharm, Changsha, Hunan, Peoples R China.;[Chen, Nai-Hong] Guangzhou Univ Chinese Med, Inst Clin Pharmacol, Guangzhou, Guangdong, Peoples R China.
通讯机构：
[Chen, Nai-Hong] C;[Chen, Nai-Hong] P;Chinese Acad Med Sci, Inst Mat Med, Beijing 100050, Peoples R China.;Peking Union Med Coll, Beijing 100050, Peoples R China.
摘要：
The abnormally hyperphosphorylated tau is thought to be implicated in diabetes-associated cognitive deficits. The role of mammalian target of rapamycin (mTOR) / S6 kinase (S6K) signalling in the formation of tau hyperphosphorylation has been previously studied. Caveolin-1 (Cav-1), the essential structure protein of caveolae, promotes neuronal survival and growth, and inhibits glucose metabolism. In this study, we aimed to investigate the role of Cav-1 in the formation of tau hyperphosphorylation under chronic hyperglycemic condition (HGC). Diabetic rats were induced by streptozotocin (STZ). Primary hippocampal neurons with or without molecular intervention such as the transient over-expression or knock-down were subjected to HGC. The obtained experimental samples were analyzed by real time quantitative RT-PCR, Western blot, immunofluorescence or immunohistochemisty. We found: 1) that a chronic HGC directly decreases Cav-1 expression, increases tau phosphorylation and activates mTOR/S6K signalling in the brain neurons of diabetic rats, 2) that overexpression of Cav-1 attenuates tau hyperphosphorylation induced by chronic HGC in primary hippocampal neurons, whereas down-regulation of Cav-1 using Cav-1 siRNA dramatically worsens tau hyperphosphorylation via mTOR/S6K signalling pathway, and 3) that the down-regulation of Cav-1 induced by HGC is independent of mTOR signalling. Our results suggest that tau hyperphosphorylation and the sustained over-activated mTOR signalling under hyperglycemia may be due to the suppression of Cav-1. Therefore, Cav-1 is a potential therapeutic target for diabetes-induced cognitive dysfunction.
期刊：
Journal of Stroke & Cerebrovascular Diseases,2017年26(10):2065-2073 ISSN：1052-3057
通讯作者：
Chen, Nai-Hong
作者机构：
[Niu, Fei; Song, Xiu-Yun; Han, Ning; Kong, Ling-Lei; Hu, Jin-Feng; Chen, Nai-Hong; Zuo, Wei; Wang, Xiao-Feng] Chinese Acad Med Sci, Peking Union Med Coll, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, 2 Nanwei Rd, Beijing 100050, Peoples R China.;[Niu, Fei; Song, Xiu-Yun; Han, Ning; Kong, Ling-Lei; Hu, Jin-Feng; Chen, Nai-Hong; Zuo, Wei; Wang, Xiao-Feng] Chinese Acad Med Sci, Peking Union Med Coll, Neurosci Ctr, 2 Nanwei Rd, Beijing 100050, Peoples R China.;[Niu, Fei] Capital Med Univ, Beijing Neurosurg Inst, Beijing 100050, Peoples R China.;[Chen, Nai-Hong] Hunan Univ Chinese Med, Coll Pharm, Changsha 410208, Hunan, Peoples R China.
通讯机构：
[Chen, Nai-Hong] C;Chinese Acad Med Sci, Peking Union Med Coll, Inst Mat Med, State Key Lab Bioact Subst & Funct Nat Med, 2 Nanwei Rd, Beijing 100050, Peoples R China.;Chinese Acad Med Sci, Peking Union Med Coll, Neurosci Ctr, 2 Nanwei Rd, Beijing 100050, Peoples R China.
摘要：
OBJECTIVE: IMM-H004 (7-hydroxy-5-methoxy-4-methyl-3-[4-methylpiperazin-1-yl]-2H-chromen-2-one) is a novel coumarin derivative that showed better effect in improving global cerebral ischemia in rats. However, the effects and mechanisms in focal cerebral ischemia were not clear. Blood-brain barrier (BBB) protection is a vital strategy for the treatment of cerebral ischemia. This study is to investigate whether IMM-H004 improves brain ischemia injury via BBB protection. METHODS: Focal brain ischemia model was induced by middle cerebral artery occlusion for 1 hour and reperfusion (MCAO/R) for 24 hours in rats. IMM-H004 (1.5, 3, 6 mg/kg) and edaravone (positive drug, 6 mg/kg) were administered after 5 minutes of occlusion. Neurological score and TTC staining were used to evaluate the effect of IMM-H004. Evans Blue (EB) staining and electron microscopy were used to assess BBB permeability. Western blot, reverse transcription-polymerase chain reaction, and immunohistochemistry were used to detect the expression of BBB structure-related proteins. RESULTS: Compared with the model group, IMM-H004 in the focal brain ischemia model improved neurological function and reduced cerebral infarction size and edema content. IMM-H004 sharply reduced the EB content and alleviated BBB structure. In addition, IMM-H004 increased the level of zonula occludens (ZO-1) and occluding, decreased the level of aquaporin 4 and matrix metalloproteinase 9, either in cortex or in hippocampus. And all of these changed were related to BBB protection. CONCLUSION: IMM-H004 improved cerebral ischemia injury via BBB protection. For a potential therapy drug of cerebral ischemia, IMM-H004 merits further study.
期刊：
Journal of Cellular Biochemistry,2017年118(10):3130-3141 ISSN：0730-2312
通讯作者：
Chen, Naihong
作者机构：
[Xia, Congyuan; Gao, Yan; Chen, Naihong; Zuo, Wei; Zhang, Zhao] Chinese Acad Med Sci, Inst Mat Med, Dept Pharmacol, State Key Lab Bioact Subst & Funct Nat Med, Beijing, Peoples R China.;[Xia, Congyuan; Gao, Yan; Chen, Naihong; Zuo, Wei; Zhang, Zhao] Peking Union Med Coll, Beijing, Peoples R China.;[Ai, Qidi; Chen, Naihong; Chu, Shifeng; Luo, Piao] Hunan Univ Chinese Med, Coll Pharm, Changsha, Hunan, Peoples R China.;[Cao, Peng] Jiangsu Acad Tradit Chinese Med, Lab Cellular & Mol Biol, 100 Shizi St,Hongshan Rd, Nanjing, Jiangsu, Peoples R China.;[Chen, Naihong] Chinese Acad Med Sci, Inst Mat Medica, Dept Pharmacol,Peking Union Med Coll, State Key Lab Bioact Subst & Funct Nat Med, Beijing, Peoples R China.
通讯机构：
[Chen, Naihong] C;Chinese Acad Med Sci, Inst Mat Medica, Dept Pharmacol,Peking Union Med Coll, State Key Lab Bioact Subst & Funct Nat Med, Beijing, Peoples R China.
作者机构：
[Hu, Jian; Huang, Li; Luo, Weihao; Duan, Lili; Zhang, Xi; Li, Jia; Hu, Zheng; He, Rongzhang; Luo, Di-Xian; Liao, Duanfang; Huang, Renbin; Guo, Yuanwei; Tan, Tan; Hu, Xinglin] Univ South China, Peoples Hosp Chenzhou 1, Natl & Local Joint Engn Lab High Throughput Mol D, Translat Med Inst, Chenzhou 423000, Peoples R China.;[Hu, Jian; Huang, Li; Luo, Di-Xian; Guo, Yuanwei; Tan, Tan] First Peoples Hosp Chenzhou, Ctr Clin Pathol, Chenzhou 423000, Peoples R China.;[Zhang, Xi] First Peoples Hosp Chenzhou, Dept Neurol, Chenzhou 423000, Peoples R China.;[Liao, Duanfang] Hunan Univ Chinese Med, Sch Pharm, Changsha 410208, Hunan, Peoples R China.;[Zhu, Yuan-Shan] Cent S Univ, Xiangya Hosp, Dept Clin Pharmacol, Changsha 410078, Hunan, Peoples R China.
通讯机构：
[Luo, Di-Xian] U;[Luo, Di-Xian] F;Univ South China, Peoples Hosp Chenzhou 1, Natl & Local Joint Engn Lab High Throughput Mol D, Translat Med Inst, Chenzhou 423000, Peoples R China.;First Peoples Hosp Chenzhou, Ctr Clin Pathol, Chenzhou 423000, Peoples R China.
关键词：
AKR1B10;ERK;breast cancer
摘要：
Background: Aldo-keto reductase family 1, member B10 (AKR1B10), is known to be significantly induced in the cells of various cancers such as breast cancer. However, the mechanisms of AKR1B10 promoting tumorigenesis in breast cancer remain unclear. In the present study, we demonstrated the potential role and mechanism of AKR1B10 in the invasion and migration of breast cancer cells. Methods: The expression level of AKR1B10 in breast carcinoma, para-carcinoma and cancer tissues were detected by immunohistochemical evaluation and real-time polymerase chain reaction (RT-PCR), and the correlationships between AKR1B10 expression and clinicopathological features in breast cancer patients (n = 131) were investigated. AKR1B10 was ectopically expressed in MCF-7 cells or silenced in BT-20 cells. The roles of AKR1B10 expression in the migration and invasion of MCF-7 cells and BT-20 cells were explored by wound healing assay, transwell migration assay and transwell matrigel invasion assay, and finally the activation level of extracellular signal-regulated kinase 1/2 (EKR1/2) activation and the expression level of matrix metalloproteinase-2 (MMP2) and vimentin in MCF-7 and BT-20 cells were measured by western blot. Results: We found that AKR1B10 expression was increased in malignant tissues, which was correlated positively with tumor size, lymph node metastasis (p<0.05). MCF-7/AKR1B10 cells displayed a higher ability of migration (43.57 +/- 1.04%) compared with MCF-7/vector cells (29.12 +/- 1.34%) in wound healing assay, and the migrated cell number of MCF-7/AKR1B10 was more (418.43 +/- 9.62) than that of MCF-7/vector (222.43 +/- 17.75) in transwell migration assay without matrigel. We furtherly confirmed MCF-7/AKR1B10 cells invaded faster compared with MCF-7/vector cells by transwell matrigel invasion assay. Finally, we found AKR1B10 induced the migration and invasion of MCF-7 and BT-20 cells by activating EKR signaling, which promoted the expressions of MMP2 and vimentin. PD98059, a specific inhibitor of the activation of MEK, blocked the migration and invasion by inhibiting the expression of MMP2 and vimentin. Conclusions: AKR1B10 is overexpressed in breast cancer, and promotes the migration and invasion of MCF-7 and BT-20 cells by activating ERK signaling pathway.
关键词：
high-mobility group box 1;lupane-type triterpenoid saponins;Acanthopanax gracilistylus;tumor necrosis factor-alpha;interleukin-1 beta;nuclear factor-kappa B
摘要：
Acanthopanax gracilistylus (AGS) has long been used in traditional Chinese medicine for the treatment of various inflammatory diseases. 3-O-beta-D-glucopyranosyl 3 alpha, 11 alpha-dihydroxylup-20(29)-en-28-oic acid, acantrifoside A, acankoreoside D, acankoreoside B and acankoreoside A are major lupane-type triterpenoid saponins derived from AGS. In the present study, these five saponins were isolated from AGS by chromatography and their anti-inflammatory activities were investigated in lipopolysaccharide (LPS)-treated RAW264.7 macrophages. Cell viability was evaluated by MTT assay. Tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta and NF-kappa B p65 were measured by ELISA. The gene expression levels of TNF-alpha and IL-1 beta was detected by reversetranscription polymerase chain reaction. And high-mobility group box 1 (HMGB1) were analyzed by western blotting. The results demonstrated that these five saponins significantly suppressed LPS-induced expression of TNF-alpha and IL-1 beta at the mRNA and protein level in RAW264.7 cells. Further analysis revealed that acankoreoside A and acankoreoside B were able to reduce the secretion of HMGB1 and NF-kappa B activity induced by LPS in RAW264.7 macrophages. Taken together, these results suggested that the anti-inflammatory activity of AGS-derived saponins may be associated with the downregulation of TNF-alpha and IL-1 beta, and the 'late-phase' proinflammatory cytokine HMGB1, via negative regulation of the NF-kappa B pathway in RAW264.7 cells.
作者机构：
[梁雪娟; 刘浩; 张水寒; 万丹] Institute of Chinese Materia Medica, Hunan Academy of Chinese Medicine, Changsha 410013, China;[梁雪娟; 刘浩; 陈林; 张水寒; 万丹; 周融融] Technology Service Center of Survey and Monitoring of Chinese Medicinal Materials in Hunan Province, Changsha 410013, China;[梁雪娟; 刘浩; 张水寒; 万丹] 3. Tsumura & Co., Tokyo 107-8521, Japan;[Koin, Toda] Tsumura & Co., Tokyo 107-8521, Japan;[黄璐琦] National Resource Center for Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China
作者机构：
[何琴] School of Pharmacy, Hunan University of Chinese Medicine, Changsha 410208, China;[何琴; 李春雨; 肖小河; 张乐; 涂灿; 刘振杰; 王伽伯; 沙孟晨] China Military Institute of Chinese Medicine, 302 Military Hospital of China, Beijing 100039, China;[涂灿; 刘振杰] School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 610000, China;[李春雨] Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Beijing 100094, China
