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Picroside Ⅱ


Catalogue Number : BF-P3027
Specification : 98%
CAS number : 39012-20-9
Formula : C23H28O13
Molecular Weight : 512.46
PUBCHEM ID : 3081484
Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow needle crystal

Botanical Source

Neopicrorhiza scrophulariiflora

Structure Type



Standards;Natural Pytochemical;API




AMPHICOSIDE/Amphicoside II/PicrosideII/Vanilloyl catalpol/Picroside-2/6'-VANILLOYL CATALPOL/2-(Hexopyranosyloxy)-1a-(hydroxymethyl)-1a,1b,2,5a,6,6a-hexahydrooxireno[4,5]cyclopenta[1,2-c]pyran-6-yl 4-hydroxy-3-methoxybenzoate/PICROSID II/Benzoic acid, 4-hydroxy-3-methoxy-, 2-(hexopyranosyloxy)-1a,1b,2,5a,6,6a-hexahydro-1a-(hydroxymethyl)oxireno[4,5]cyclopenta[1,2-c]pyran-6-yl ester


[2-(hydroxymethyl)-10-[3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-3,9-dioxatricyclo[,4]dec-7-en-5-yl] 4-hydroxy-3-methoxybenzoate


1.7±0.1 g/cm3



Flash Point

267.9±26.4 °C

Boiling Point

780.8±60.0 °C at 760 mmHg

Melting Point



InChl Key


WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:39012-20-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




Introduction: Many structural and functional damages are observed in cells and tissues after reperfusion of previously viable ischemic tissues. Acute ischemia reperfusion (I/R) injury of lower extremities occurs especially when a temporary cross-clamp is applied to the abdominal aorta during aortic surgery. Research regarding the treatment of I/R injury has been increasing day-by-day. In this study, we aimed to investigate the effect of picroside II on skeletal muscle of rats experiencing simulated I/R.
Materials and methods: Twenty-four male Wistar albino rats weighing between 210 and 300 g were used in this study. Rats were randomly divided into 4 groups of 6 rats each (control, I/R, control + picroside II, and I/R + picroside II). The infrarenal section of the abdominal aorta was occluded with an atraumatic microvascular clamp in I/R group. The clamp was removed after 120 minutes and reperfusion was provided for a further 120 minutes. Picroside II (10 mg kg-1) was administered intraperitoneally to the animals in control + picroside II and I/R + picroside II groups. At the end of the study, skeletal muscle tissue was obtained for the determination of total oxidant status (TOS) and total antioxidant status (TAS) levels. Apoptosis was evaluated by TUNEL experiment.
Results: TOS levels were significantly higher in I/R group than that of control and I/R + picroside II groups (P=0.014, P=0.005, respectively). TAS levels were significantly higher in I/R group than that of control and I/R + picroside II groups (P=0.007 P=0.005, respectively). TUNEL assay revealed that picroside II reduced cell necrosis.
Conclusion: The results of this study demonstrated that picroside II plays a critical role to prevent I/R injury. Even though our results were found to be satisfactory, it should be encouraging to those who want to conduct future research on this topic.


TAS; TOS; hind limb skeletal muscle; ischemia reperfusion; picroside II.


Effect of Picroside II on Hind Limb Ischemia Reperfusion Injury in Rats


Yigit Kılıc 1 , Abdullah ozer 1 , Tolga Tatar 1 , Mustafa Hakan Zor 1 , Mehmet KiriSci 2 , Hakan Kartal 3 , Ali Dogan Dursun 4 , Deniz Billur 5 , Mustafa Arslan 6 , AySegul Kucuk 7

Publish date

2017 Jun 26




Background and purpose: Thrombolysis is used to improve cerebral circulation; at the same time, neuroprotective drugs such as antioxidants should also be used. The aim of these experiments was to explore the protective mechanism of an antioxidant, picroside II, on the blood-brain barrier (BBB) after cerebral ischemia-reperfusion (CI/R) injury.
Methods: To observe the antagonistic effect of picroside II on CI/R damage, the neurological deficit score and the infarct volume were measured. To detect the protective effect of picroside II on nerve cells and the BBB, the morphology and structure of cortical brain tissue were observed, respectively. To investigate the antioxidant effect and mechanism of picroside II, reactive oxygen species (ROS) content, the activity of Nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), and the protein levels of Nox2 and Rac-1 were detected. To investigate the protective mechanism of picroside II on the BBB, the levels of ROCK, MLCK, MMP-2 and claudin-5 were tested.
Results: A higher neurological score, bigger cortex infarction, more damaged neuron structure and injured BBB, increased content of ROS and activity of NADPH oxidase, higher protein levels of Nox2, Rac-1, ROCK, MLCK and MMP-2 and lower levels of claudin-5 were observed in the model group. In the picroside group, the neurological score, neuronal damage, BBB injury, ROS content and NADPH oxidase activity were reduced (P<0.05), and the protein levels of Rac-1, Nox2, ROCK, MLCK and MMP-2 were down-regulated (P<0.05), while the expression of claudin-5 was up-regulated (P<0.05).
Conclusions: Picroside II could protect the nervous system possibly through reducing the content of ROS by down-regulating the expression of Rac-1 and Nox2 and could protect the BBB through reducing the expression of ROCK, MLCK, and MMP-2, while enhancing the expression of claudin-5.


TAS; TOS; hind limb skeletal muscle; ischemia reperfusion; picroside II.


Picroside II Protects the Blood-Brain Barrier by Inhibiting the Oxidative Signaling Pathway in Cerebral Ischemia-Reperfusion Injury


Li Zhai 1 , Min Liu 1 , Tingting Wang 2 , Hongyan Zhang 2 , Shan Li 2 , Yunliang Guo 2

Publish date

2017 Apr 7




Picroside II, one of the major components isolated from the seed of natural plant picrorhiza, is widely used in traditional Chinese medicine. The present study was performed to define effects of picroside II on nuclear factor-kappaB ligand (RANKL)-stimulated osteoclast differentiation in vitro and on lipopolysaccharide (LPS)-induced bone loss in vivo. The bone marrow cells (BMMs) were harvested and induced with RANKL followed by treatment with picroside II at several doses, and the differentiation of osteoclasts from these cells was evaluated by tartrate-resistant acid phosphatase (TRAP) staining and resorption pit formation assay. The effects of picroside II on osteoclastogenesis were studied by examining RANKL-induced osteoclast F-actin ring formation and osteoclast bone resorption. Moreover, we explored the mechanisms of these downregulation effects by performed Western blotting and quantitative RT-PCR examination. Results demonstrated picroside II strongly inhibited RANKL-induced osteoclast formation when added during the early stage of BMMs cultures, suggesting that it acts on osteoclast precursors to inhibit RANKL/RANK signaling. Moreover, picroside II markedly decreased the phosphorylation of p38, ERK, JNK, p65, and I-κB degradation, and significantly suppressed c-Fos and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), both the key transcription factors during osteoclastogenesis. Furthermore, in vivo studies verified the bone protection effects of picroside II. These results collectively suggested that picroside II acted as an anti-resorption agent by blocking osteoclast activation. J. Cell. Biochem. 118: 4479-4486, 2017. © 2017 Wiley Periodicals, Inc.




Picroside II Inhibits RANKL-Mediated Osteoclastogenesis by Attenuating the NF-κB and MAPKs Signaling Pathway In Vitro and Prevents Bone Loss in Lipopolysaccharide Treatment Mice


Xiaobin Yang 1 , Wenjie Gao 1 , Biao Wang 1 , Xiaodong Wang 1 , Hua Guo, Yuan Xiao 1 , Lingbo Kong 1 , Dingjun Hao 1

Publish date

2017 Dec