AP2/ERF转录因子在调控植物的生长发育、抵抗生物和非生物胁迫方面发挥重要作用。克隆ShERF3,并分析其功能,为甘蔗抗逆遗传改良提供基因资源。基于转录组数据从‘新台糖22号’甘蔗中克隆ShERF3,并通过Real time PCR、生物信息学分析、...AP2/ERF转录因子在调控植物的生长发育、抵抗生物和非生物胁迫方面发挥重要作用。克隆ShERF3,并分析其功能,为甘蔗抗逆遗传改良提供基因资源。基于转录组数据从‘新台糖22号’甘蔗中克隆ShERF3,并通过Real time PCR、生物信息学分析、水稻原生质体亚细胞定位等技术对ShERF3编码的蛋白特性、亚细胞定位及基因表达模式进行分析。结果显示,克隆获得1 142 bp ShERF3的cDNA序列,包含1个1 053 bp的完整开放阅读框,编码350个氨基酸;ShERF3蛋白含有一个AP2结构域,属于AP2/ERF家族ERF亚家族成员,与高粱和柳枝稷ERF3、谷子和哈氏黍ERF118蛋白同源性较高;ShERF3蛋白是一种不稳定的疏水性蛋白,亚细胞定位结果显示其定位于细胞核;ShERF3主要在甘蔗成熟茎节中表达,在叶片和根系中相对表达较低;在PEG处理下,ShERF3表达先下调后上调,在NaCl处理下,随着胁迫时间延长ShERF3表达量降低。甘蔗ShERF3积极响应干旱和盐逆境胁迫,可能在甘蔗茎秆发育、干旱以及盐胁迫应答方面发挥关键作用。展开更多
With the internationally growing popularity of traditional Chinese medicine(TCM), TCM-induced nephropathy has attracted public attention. Minimizing this toxicity is an important issue for future research. Typical nep...With the internationally growing popularity of traditional Chinese medicine(TCM), TCM-induced nephropathy has attracted public attention. Minimizing this toxicity is an important issue for future research. Typical nephrotoxic TCM drugs such as Aristolochic acid, Tripterygium wilfordii Hook. f, Rheum officinale Baill, and cinnabar mainly damage renal proximal tubules or cause interstitial nephritis. Transporters in renal proximal tubule are believed to be critical in the disposition of xenobiotics. In this review, we provide information on the alteration of renal transporters by nephrotoxic TCMs, which may be helpful for understanding the nephrotoxic mechanism of TCMs and reducing adverse effects. Studies have proven that when administering nephrotoxic TCMs, the expression or function of renal transporters is altered, especially organic anion transporter 1 and 3. The alteration of these transporters may enhance the accumulation of toxic drugs or the dysfunction of endogenous toxins and subsequently sensitize the kidney to injury.Transporters-related drug combination and clinical biomarkers supervision to avoid the risk of future toxicity are proposed.展开更多
Objective： To explore the delayed neuroprotection induced by paeoniflorin（PF）, the principal component of Paeoniae radix prescribed in Chinese medicine, and its underlying mechanisms in rats subjected to vascular d...Objective： To explore the delayed neuroprotection induced by paeoniflorin（PF）, the principal component of Paeoniae radix prescribed in Chinese medicine, and its underlying mechanisms in rats subjected to vascular dementia（VD）. Methods： A rat model of VD was induced by bilateral common carotid arteries occlusion（BCCAO）. Low-dose or high-dose PF（20 or 40 mg/kg once per day） was administrated for 28 days after VD. The behavioral analysis of rat was measured by water morris. Regional cerebral blood volume（r CBV）, regional cerebral blood flow（r CBF） and mean transit time（MTT） were measured in the bilateral hippocampus by perfusion-weighted imaging（PWI）. The levels of interleukin-1β（IL-1β）, interleukin-6（IL-6）, and tumor necrosis factor alpha（TNF-α） were measured by commercially available enzyme-linked immunosorbent assay kits. Protein levels were evaluated by western blot analysis. m RNA levels were evaluated by real time-polymerase chain reaction. Western blotting was used to estimate p65 translocation. Results： The behavioral analysis showed that PF could decrease the escape latency time（P〈0.05）, and increase the residence time of the original platform quadrant and the across platform frequency in water maze in VD rats（P〈0.05）. Likewise, PF remarkably promoted the r CBV（P〈0.05）, r CBF and decreased per minute MTT（P〈0.05） in hippocampus of VD rats. Furthermore, PF decreased the release of IL-1β, IL-6 and TNF-α as well as inhibited the m RNA expression of IL-1β, IL-6 and TNF-α in the hippocampus of VD rats（P〈0.05 or P〈0.01）. PF also could decrease the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2 in the hippocampus of VD rats（P〈0.05 or P〈0.01）. In addition, PF significantly inhibited the nuclear factor κB（NF-κB） pathway in the hippocampus of VD rats. Conclusions： PF significantly attenuates cognitive impairment, improves hippocampus perfusion and inhibits inflammatory response in VD rats. In addition, the anti-inflammatory effects of PF might be due to inhibiting the NF-κB pathway. PF may be a potential clinical application in improving VD.展开更多
基金Projects(51974055, 42122052) supported by the National Natural Science Foundation of ChinaProject(2021JLM-11) supported by the Joint Fund of Natural Science Basic Research Program of Shaanxi Province,China+1 种基金Project(202001AT070150) supported by Yunnan Fundamental Research Projects,ChinaProject(2020D-5007-0302) supported by the Fund of China Petroleum Technology and Innovation。
文摘AP2/ERF转录因子在调控植物的生长发育、抵抗生物和非生物胁迫方面发挥重要作用。克隆ShERF3,并分析其功能,为甘蔗抗逆遗传改良提供基因资源。基于转录组数据从‘新台糖22号’甘蔗中克隆ShERF3,并通过Real time PCR、生物信息学分析、水稻原生质体亚细胞定位等技术对ShERF3编码的蛋白特性、亚细胞定位及基因表达模式进行分析。结果显示,克隆获得1 142 bp ShERF3的cDNA序列,包含1个1 053 bp的完整开放阅读框,编码350个氨基酸;ShERF3蛋白含有一个AP2结构域,属于AP2/ERF家族ERF亚家族成员,与高粱和柳枝稷ERF3、谷子和哈氏黍ERF118蛋白同源性较高;ShERF3蛋白是一种不稳定的疏水性蛋白,亚细胞定位结果显示其定位于细胞核;ShERF3主要在甘蔗成熟茎节中表达,在叶片和根系中相对表达较低;在PEG处理下,ShERF3表达先下调后上调,在NaCl处理下,随着胁迫时间延长ShERF3表达量降低。甘蔗ShERF3积极响应干旱和盐逆境胁迫,可能在甘蔗茎秆发育、干旱以及盐胁迫应答方面发挥关键作用。
基金National Natural Science Foundation of China(Nos.81673684,81703626,81573690)Double First-Class University projects(No.CPU2018GY33)。
文摘With the internationally growing popularity of traditional Chinese medicine(TCM), TCM-induced nephropathy has attracted public attention. Minimizing this toxicity is an important issue for future research. Typical nephrotoxic TCM drugs such as Aristolochic acid, Tripterygium wilfordii Hook. f, Rheum officinale Baill, and cinnabar mainly damage renal proximal tubules or cause interstitial nephritis. Transporters in renal proximal tubule are believed to be critical in the disposition of xenobiotics. In this review, we provide information on the alteration of renal transporters by nephrotoxic TCMs, which may be helpful for understanding the nephrotoxic mechanism of TCMs and reducing adverse effects. Studies have proven that when administering nephrotoxic TCMs, the expression or function of renal transporters is altered, especially organic anion transporter 1 and 3. The alteration of these transporters may enhance the accumulation of toxic drugs or the dysfunction of endogenous toxins and subsequently sensitize the kidney to injury.Transporters-related drug combination and clinical biomarkers supervision to avoid the risk of future toxicity are proposed.
基金Supported by Excellent Adult and Young Scientist Science Foundation of Shandong Province(No.BS2010YY056)the National Key Grant of Basic Research Project(No.2010CB530403)
文摘Objective： To explore the delayed neuroprotection induced by paeoniflorin（PF）, the principal component of Paeoniae radix prescribed in Chinese medicine, and its underlying mechanisms in rats subjected to vascular dementia（VD）. Methods： A rat model of VD was induced by bilateral common carotid arteries occlusion（BCCAO）. Low-dose or high-dose PF（20 or 40 mg/kg once per day） was administrated for 28 days after VD. The behavioral analysis of rat was measured by water morris. Regional cerebral blood volume（r CBV）, regional cerebral blood flow（r CBF） and mean transit time（MTT） were measured in the bilateral hippocampus by perfusion-weighted imaging（PWI）. The levels of interleukin-1β（IL-1β）, interleukin-6（IL-6）, and tumor necrosis factor alpha（TNF-α） were measured by commercially available enzyme-linked immunosorbent assay kits. Protein levels were evaluated by western blot analysis. m RNA levels were evaluated by real time-polymerase chain reaction. Western blotting was used to estimate p65 translocation. Results： The behavioral analysis showed that PF could decrease the escape latency time（P〈0.05）, and increase the residence time of the original platform quadrant and the across platform frequency in water maze in VD rats（P〈0.05）. Likewise, PF remarkably promoted the r CBV（P〈0.05）, r CBF and decreased per minute MTT（P〈0.05） in hippocampus of VD rats. Furthermore, PF decreased the release of IL-1β, IL-6 and TNF-α as well as inhibited the m RNA expression of IL-1β, IL-6 and TNF-α in the hippocampus of VD rats（P〈0.05 or P〈0.01）. PF also could decrease the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2 in the hippocampus of VD rats（P〈0.05 or P〈0.01）. In addition, PF significantly inhibited the nuclear factor κB（NF-κB） pathway in the hippocampus of VD rats. Conclusions： PF significantly attenuates cognitive impairment, improves hippocampus perfusion and inhibits inflammatory response in VD rats. In addition, the anti-inflammatory effects of PF might be due to inhibiting the NF-κB pathway. PF may be a potential clinical application in improving VD.
