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(-)-Usnic acid

Naturally occurring dibenzofuran derivative CAS# 7562-61-0

(-)-Usnic acid

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Chemical structure

(-)-Usnic acid

3D structure

Chemical Properties of (-)-Usnic acid

Cas No. 7562-61-0 SDF Download SDF
PubChem ID 442614 Appearance Yellow powder
Formula C18H16O7 M.Wt 344.3
Type of Compound Phenols Storage Desiccate at -20°C
Synonyms (+)-Usniacin;(+)-Usnic acid
Solubility >8.025mg/mL in DMSO
Chemical Name (9bS)-2,6-diacetyl-3,7,9-trihydroxy-8,9b-dimethyldibenzofuran-1-one
SMILES CC1=C(C(=C2C(=C1O)C3(C(=CC(=C(C3=O)C(=O)C)O)O2)C)C(=O)C)O
Standard InChIKey WEYVVCKOOFYHRW-GOSISDBHSA-N
Standard InChI InChI=1S/C18H16O7/c1-6-14(22)12(8(3)20)16-13(15(6)23)18(4)10(25-16)5-9(21)11(7(2)19)17(18)24/h5,21-23H,1-4H3/t18-/m1/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of (-)-Usnic acid

1 Cladonia sp. 2 Usnea sp.

Biological Activity of (-)-Usnic acid

DescriptionUsnic acid has antitumoral, acaricidal, larvicidal, antiviral, antibiotic, antipyretic, analgesic,gastroprotective, antioxidative and anti-inflammatory activities. Use of reconstituted bovine type-I collagen-based films containing usnic acid can improve burn healing process in rats. Usnic acid perturbs various interrelated signaling pathways and that autophagy induction is a defensive mechanism against usnic acid-induced cytotoxicity; it disturbs calcium homeostasis, induces ER stress, and that Usnic acid-induced cellular damage occurs at least partially via activation of the Ca(2+) channel of SOCE.
TargetsCalcium Channel | Autophagy | Caspase | JNK | SOD | TNF-α | IL Receptor | NOS | Antifection
In vitro

Acaricidal activity of usnic acid and sodium usnic acid against Psoroptes cuniculi in vitro.[Pubmed: 24770718]

Parasitol Res. 2014 Jun;113(6):2387-90.

Usnic acid, a major active compound in lichens, was first isolated in 1884. Since then, Usnic acid and its sodium salt (sodium Usnic acid) have been used in medicine, perfumery, cosmetics, and other industries due to its extensive biological activities. However, its acaricidal activity has not been studied. In this paper, we investigated the acaricidal activity of Usnic acid and sodium Usnic acid against Psoroptes cuniculi in vitro.
METHODS AND RESULTS:
After evaluating the acaricidal activity and toxicity of Usnic acid and sodium Usnic acid in vitro, the results showed that at doses of 250, 125, and 62.5 mg/ml, Usnic acid and sodium Usnic acid can kill mites with 91.67, 85.00, and 55.00% and 100, 100, and 60.00% mortality after treatment 24 h. The LT50 values were 4.208, 8.249, and 16.950 h and 3.712, 7.339, and 15.773 h for Usnic acid and sodium Usnic acid, respectively.
CONCLUSIONS:
Sodium Usnic acid has a higher acaricidal activity than Usnic acid, which may be related to the difference in their structures.

Identification and quantitation of usnic acid from the lichen Usnea species of Anatolia and antimicrobial activity.[Pubmed: 17294685]

Z Naturforsch C. 2006 Nov-Dec;61(11-12):773-6.

Six species of lichens, such as Usnea florida, Usnea barbata, Usnea longissima, Usnea rigida, Usnea hirta and Usnea subflorida, were collected from different areas of Anatolia (district of Antalya, Karabük, Qankiri, Giresun and Trabzon) in Turkey.
METHODS AND RESULTS:
Their Usnic acid amounts in acetone extracts were determined by HPLC. In addition, antimicrobial activities of these extracts were determined against Escherichia coli (ATCC 35218), Enterococcus faecalis (RSKK 508), Proteus mirabilis (Pasteur Ens. 235), Staphylococcus aureus, Bacillus subtilis and Bacillus megaterium.
CONCLUSIONS:
It was shown that with increasing amount of Usnic acid, the antimicrobial activity increased. Usnic acid contents of Usnea species varied between 0.22-6.49% of dry weight.

Larvicidal Activity of Cladonia substellata Extract and Usnic Acid against Aedes aegypti and Artemia salina[Reference: WebLink]

Lat. Am. J. Pharm., 2009, 300(2): R349-60.

The chloroform extract of Cladonia substellata Vainio was assayed against larvae of Aedes ae- gypti, the mosquito vector of Dengue fever and Artemia salina.
METHODS AND RESULTS:
The extract was tested at concentrations ranging from 1 to 15 ppm in an aqueous medium for 24 h. LC50 and LC90 were evaluated. Since the chlo- roform extract proved to be lethal for third to fourth instar larvae, downstream processing was undertak- en to purify the active agents in the extract. The major compound in the chloroform extract was purified by crystallization followed by column chromatography to yield yellow crystals. Furthermore, Usnic acid (UA) was evaluated for its larvicidal potential. The major compound in the chloroform extract, UA, exhib- ited LC50 of 6.6 ppm (6.1 to 7.0 ppm). Therefore, UA is most likely the active principle in C. substellata.
CONCLUSIONS:
UA showed to be toxic to A. salina, a reference organism in assays to evaluate the potential toxicity hazard to invertebrates in ecosystems.

In vivo

Usnic acid protects LPS-induced acute lung injury in mice through attenuating inflammatory responses and oxidative stress.[Pubmed: 25068825]

Int Immunopharmacol. 2014 Oct;22(2):371-8.

Usnic acid is a dibenzofuran derivative found in several lichen species, which has been shown to possess several activities, including antiviral, antibiotic, antitumoral, antipyretic, analgesic, antioxidative and anti-inflammatory activities. However, there were few reports on the effects of Usnic acid on LPS-induced acute lung injury (ALI). The aim of our study was to explore the effect and possible mechanism of Usnic acid on LPS-induced lung injury.
METHODS AND RESULTS:
In the present study, we found that pretreatment with Usnic acid significantly improved survival rate, pulmonary edema. In the meantime, protein content and the number of inflammatory cells in bronchoalveolar lavage fluid (BALF) significantly decreased, and the levels of MPO, MDA, and H2O2 in lung tissue were markedly suppressed after treatment with Usnic acid. Meanwhile, the activities of SOD and GSH in lung tissue significantly increased after treatment with Usnic acid. Additionally, to evaluate the anti-inflammatory activity of Usnic acid, the expression of pro-inflammatory cytokines including tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and anti-inflammatory cytokine IL-10, and chemokines interleukin-8 (IL-8) and macrophage inflammatory protein-2 (MIP-2) in BALF were studied. The results in the present study indicated that Usnic acid attenuated the expression of TNF-α, IL-6, IL-8 and MIP-2. Meanwhile, the improved level of IL-10 in BALF was observed.
CONCLUSIONS:
In conclusion, these data showed that the protective effect of Usnic acid on LPS-induced ALI in mice might relate to the suppression of excessive inflammatory responses and oxidative stress in lung tissue. Thus, it was suggested that Usnic acid might be a potential therapeutic agent for ALI.

Collagen-based films containing liposome-loaded usnic acid as dressing for dermal burn healing.[Pubmed: 21274404]

J Biomed Biotechnol. 2011;2011:761593.

The aim of this study was assess the effect of collagen-based films containing Usnic acid as a wound dressing for dermal burn healing.
METHODS AND RESULTS:
Second-degree burn wounds were performed in forty-five Wistar rats, assigned into nine groups: COL-animals treated with collagen-based films; PHO-animals treated with collagen films containing empty liposomes; UAL-animals treated with collagen-based films containing Usnic acid incorporated into liposomes. After 7, 14, and 21 days the animals were euthanized. On 7th day there was a moderate infiltration of neutrophils, in UAL, distributed throughout the burn wounds, whereas in COL and PHO, the severity of the reaction was slighter and still limited to the margins of the burn wounds. On the 14th day, the inflammatory reaction was less intense in UAL, with remarkable plasma cells infiltration. On the 21st day, there was reduction of the inflammation, which was predominantly composed of plasma cells in all groups, particularly in UAL. The use of the Usnic acid provided more rapid substitution of type-III for type-I collagen on the 14th day, and improved the collagenization density on the 21st day.
CONCLUSIONS:
It was concluded that the use of reconstituted bovine type-I collagen-based films containing Usnic acid improved burn healing process in rats.

Protocol of (-)-Usnic acid

Kinase Assay

The role of autophagy in usnic acid-induced toxicity in hepatic cells.[Pubmed: 25078063]

Endoplasmic Reticulum Stress and Store-Operated Calcium Entry Contribute to Usnic Acid-Induced Toxicity in Hepatic Cells.[Pubmed: 25870318 ]

Toxicol Sci. 2015 Jul;146(1):116-26.

The use of Usnic acid as a weight loss agent is a safety concern due to reports of acute liver failure in humans. Previously we demonstrated that Usnic acid induces apoptosis and cytotoxicity in hepatic HepG2 cells. We also demonstrated that Usnic acid induces autophagy as a survival mechanism against its cytotoxicity. In this study, we investigated and characterized further molecular mechanisms underlying the toxicity of Usnic acid in HepG2 cells.
METHODS AND RESULTS:
We found that Usnic acid causes endoplasmic reticulum (ER) stress demonstrated by the increased expression of typical ER stress markers, including CHOP, ATF-4, p-eIF2α, and spliced XBP1. Usnic acid inhibited the secretion of Gaussia luciferase measured by an ER stress reporter assay. An ER stress inhibitor 4-phenylbutyrate attenuated Usnic acid-induced apoptosis. Moreover, Usnic acid significantly increased the cytosolic free Ca(2+) concentration. Usnic acid increased the expression of calcium release-activated calcium channel protein 1 (CRAM1 or ORAI1) and stromal interaction molecule 1, two key components of store-operated calcium entry (SOCE), which is the major Ca(2+) influx pathway in non-excitable cells, this finding was also confirmed in primary rat hepatocytes. Furthermore, knockdown of ORAI1 prevented ER stress and ATP depletion in response to Usnic acid. In contrast, overexpression of ORAI1 increased ER stress and ATP depletion caused by Usnic acid.
CONCLUSIONS:
Taken together, our results suggest that Usnic acid disturbs calcium homeostasis, induces ER stress, and that Usnic acid-induced cellular damage occurs at least partially via activation of the Ca(2+) channel of SOCE.

Toxicol Sci. 2014 Nov;142(1):33-44.

The use of Usnic acid and Usnic acid-containing products is associated with acute liver failure; however, mechanistic studies of hepatotoxicity caused by Usnic acid are limited. In this study, we investigated and characterized the possible mechanisms, especially the role of autophagy in Usnic acid's toxicity in human HepG2 cells.
METHODS AND RESULTS:
Usnic acid caused apoptosis as demonstrated by an increased caspase-3/7 activity and an increased subdiploid nucleus formation. Usnic acid-induced autophagy as demonstrated by the conversion of LC3B-I to LC3B-II, degradation of P62, and an increased number of puncta. Inhibition of autophagy by treating cells with autophagy inhibitors (3-methyladenine or chloroquine) or by small interfering RNA against Atg7 aggravated Usnic acid-induced apoptosis and decreased cell viability, indicating that autophagy plays a protective role against Usnic acid-induced toxicity. Moreover, Usnic acid activated the MAPK signaling pathway. Usnic acid-elicited apoptosis was enhanced and autophagy was decreased when JNK was suppressed by a specific inhibitor. Additionally, inhibition of autophagy decreased the activity of JNK.
CONCLUSIONS:
Taken together, our results suggest that Usnic acid perturbs various interrelated signaling pathways and that autophagy induction is a defensive mechanism against Usnic acid-induced cytotoxicity.

Animal Research

Gastroprotective and antioxidant effects of usnic acid on indomethacin-induced gastric ulcer in rats.[Pubmed: 16169175 ]

J Ethnopharmacol. 2006 Jan 3;103(1):59-65.

Usnea longissima, a medicinal lichen of Anatolia (Turkey), is used in the treatment of gastric ulcer in local folk medicine.
METHODS AND RESULTS:
In this paper, the gastroprotective effect of Usnic acid (UA) isolated from Usnea longissima was investigated in the indomethacin-induced gastric ulcers in rats at doses of 25, 50, 100 and 200 mg/kg body weight. The gastric lesions were significantly reduced by all doses of UA as compared with the indomethacin (25 mg/kg body weight) treated group. In the stomach tissues of treated animals, the in vivo antioxidant levels were evaluated. The administration of indomethacin caused a significant decrease in the levels of superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH), and an increase in the lipid peroxidation (LPO) level (p < 0.05). The administration of all doses of UA reversed the trend, inducing a significant increase of SOD, GSH and GPx levels and a reduction in LPO level in tissues. However, catalase (CAT), glutathione reductase (GR) and myeloperoxidase (MPx) activities, increased by indomethacin, were found to be lower in the UA- and ranitidine-treated groups. The gastric mucosal constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) activities were also investigated in tissues of UA- (100 mg/kg), ranitidine- (50 mg/kg) and indomethacin-treated rat groups. The administration of UA and ranitidine increased the cNOS activity and lowered the iNOS activity as compared with indomethacin-treated group.
CONCLUSIONS:
These results suggest that the gastroprotective effect of UA can be attributed to its reducing effect on the oxidative damage and neutrophil infiltration in tissues.

(-)-Usnic acid Dilution Calculator

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Preparing Stock Solutions of (-)-Usnic acid

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.9044 mL 14.5222 mL 29.0444 mL 58.0889 mL 72.6111 mL
5 mM 0.5809 mL 2.9044 mL 5.8089 mL 11.6178 mL 14.5222 mL
10 mM 0.2904 mL 1.4522 mL 2.9044 mL 5.8089 mL 7.2611 mL
50 mM 0.0581 mL 0.2904 mL 0.5809 mL 1.1618 mL 1.4522 mL
100 mM 0.029 mL 0.1452 mL 0.2904 mL 0.5809 mL 0.7261 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on (-)-Usnic acid

MIC: 0.05 μg/62.5 μl to 3.1 μg/62.5 μl

Microorganisms can colonize a wide variety of medical devices, putting patients at risk for systemic and local infectious complications, including local-site infections, endocarditis, and catheter-related bloodstream infections. (+)-Usniacin is a secondary lichen metabolite that possesses antimicrobial activity against various planktonic gram-positive bacteria.

In vitro: (+)-Usniacin showed antimicrobial activity against the same microorganisms as that of acetone extract. Among the three analogues it was the most active one having quite low MIC values. Furthermore, (+)-Usniacin did not show any activity against A. hydrophila and B. cereus whereas (D)-usnic acid did. On the other hand, (+)-Usniacin was active against Y. enterocolitica whereas (D)-usnic acid was not active [1].

In vivo: No animal in-vivo study has been reproted so far.

Clinical trials: Trials carried out in volunteers showed that mouth-rinse with (+)-Usniacin preparations exerted a selective and long lasting action against S. mutans. The adherence of S. mutans to smooth surfaces was not increased by the presence of subinhibiting concentrations of (+)-Usniacin. These characteristics make (+)-Usniacin a suitable candidate for topical use in oral medicine [2].

References:
[1] Tay T, Türk AO, Yilmaz M, Türk H, Kivanç M.  Evaluation of the antimicrobial activity of the acetone extract of the lichen Ramalina farinacea and its (+)-usnic acid, norstictic acid, and protocetraric acid constituents. Z Naturforsch C. 2004 May-Jun;59(5-6):384-8.
[2] Ghione M, Parrello D, Grasso L.   Usnic acid revisited, its activity on oral flora. Chemioterapia. 1988 Oct;7(5):302-5.

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References on (-)-Usnic acid

The role of autophagy in usnic acid-induced toxicity in hepatic cells.[Pubmed:25078063]

Toxicol Sci. 2014 Nov;142(1):33-44.

The use of usnic acid and usnic acid-containing products is associated with acute liver failure; however, mechanistic studies of hepatotoxicity caused by usnic acid are limited. In this study, we investigated and characterized the possible mechanisms, especially the role of autophagy in usnic acid's toxicity in human HepG2 cells. Usnic acid caused apoptosis as demonstrated by an increased caspase-3/7 activity and an increased subdiploid nucleus formation. Usnic acid-induced autophagy as demonstrated by the conversion of LC3B-I to LC3B-II, degradation of P62, and an increased number of puncta. Inhibition of autophagy by treating cells with autophagy inhibitors (3-methyladenine or chloroquine) or by small interfering RNA against Atg7 aggravated usnic acid-induced apoptosis and decreased cell viability, indicating that autophagy plays a protective role against usnic acid-induced toxicity. Moreover, usnic acid activated the MAPK signaling pathway. Usnic acid-elicited apoptosis was enhanced and autophagy was decreased when JNK was suppressed by a specific inhibitor. Additionally, inhibition of autophagy decreased the activity of JNK. Taken together, our results suggest that usnic acid perturbs various interrelated signaling pathways and that autophagy induction is a defensive mechanism against usnic acid-induced cytotoxicity.

Identification and quantitation of usnic acid from the lichen Usnea species of Anatolia and antimicrobial activity.[Pubmed:17294685]

Z Naturforsch C. 2006 Nov-Dec;61(11-12):773-6.

Six species of lichens, such as Usnea florida, Usnea barbata, Usnea longissima, Usnea rigida, Usnea hirta and Usnea subflorida, were collected from different areas of Anatolia (district of Antalya, Karabuk, Qankiri, Giresun and Trabzon) in Turkey. Their usnic acid amounts in acetone extracts were determined by HPLC. In addition, antimicrobial activities of these extracts were determined against Escherichia coli (ATCC 35218), Enterococcus faecalis (RSKK 508), Proteus mirabilis (Pasteur Ens. 235), Staphylococcus aureus, Bacillus subtilis and Bacillus megaterium. It was shown that with increasing amount of usnic acid, the antimicrobial activity increased. Usnic acid contents of Usnea species varied between 0.22-6.49% of dry weight.

Usnic acid protects LPS-induced acute lung injury in mice through attenuating inflammatory responses and oxidative stress.[Pubmed:25068825]

Int Immunopharmacol. 2014 Oct;22(2):371-8.

Usnic acid is a dibenzofuran derivative found in several lichen species, which has been shown to possess several activities, including antiviral, antibiotic, antitumoral, antipyretic, analgesic, antioxidative and anti-inflammatory activities. However, there were few reports on the effects of usnic acid on LPS-induced acute lung injury (ALI). The aim of our study was to explore the effect and possible mechanism of usnic acid on LPS-induced lung injury. In the present study, we found that pretreatment with usnic acid significantly improved survival rate, pulmonary edema. In the meantime, protein content and the number of inflammatory cells in bronchoalveolar lavage fluid (BALF) significantly decreased, and the levels of MPO, MDA, and H2O2 in lung tissue were markedly suppressed after treatment with usnic acid. Meanwhile, the activities of SOD and GSH in lung tissue significantly increased after treatment with usnic acid. Additionally, to evaluate the anti-inflammatory activity of usnic acid, the expression of pro-inflammatory cytokines including tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6) and anti-inflammatory cytokine IL-10, and chemokines interleukin-8 (IL-8) and macrophage inflammatory protein-2 (MIP-2) in BALF were studied. The results in the present study indicated that usnic acid attenuated the expression of TNF-alpha, IL-6, IL-8 and MIP-2. Meanwhile, the improved level of IL-10 in BALF was observed. In conclusion, these data showed that the protective effect of usnic acid on LPS-induced ALI in mice might relate to the suppression of excessive inflammatory responses and oxidative stress in lung tissue. Thus, it was suggested that usnic acid might be a potential therapeutic agent for ALI.

Collagen-based films containing liposome-loaded usnic acid as dressing for dermal burn healing.[Pubmed:21274404]

J Biomed Biotechnol. 2011;2011:761593.

The aim of this study was assess the effect of collagen-based films containing usnic acid as a wound dressing for dermal burn healing. Second-degree burn wounds were performed in forty-five Wistar rats, assigned into nine groups: COL-animals treated with collagen-based films; PHO-animals treated with collagen films containing empty liposomes; UAL-animals treated with collagen-based films containing usnic acid incorporated into liposomes. After 7, 14, and 21 days the animals were euthanized. On 7th day there was a moderate infiltration of neutrophils, in UAL, distributed throughout the burn wounds, whereas in COL and PHO, the severity of the reaction was slighter and still limited to the margins of the burn wounds. On the 14th day, the inflammatory reaction was less intense in UAL, with remarkable plasma cells infiltration. On the 21st day, there was reduction of the inflammation, which was predominantly composed of plasma cells in all groups, particularly in UAL. The use of the usnic acid provided more rapid substitution of type-III for type-I collagen on the 14th day, and improved the collagenization density on the 21st day. It was concluded that the use of reconstituted bovine type-I collagen-based films containing usnic acid improved burn healing process in rats.

Endoplasmic Reticulum Stress and Store-Operated Calcium Entry Contribute to Usnic Acid-Induced Toxicity in Hepatic Cells.[Pubmed:25870318]

Toxicol Sci. 2015 Jul;146(1):116-26.

The use of usnic acid as a weight loss agent is a safety concern due to reports of acute liver failure in humans. Previously we demonstrated that usnic acid induces apoptosis and cytotoxicity in hepatic HepG2 cells. We also demonstrated that usnic acid induces autophagy as a survival mechanism against its cytotoxicity. In this study, we investigated and characterized further molecular mechanisms underlying the toxicity of usnic acid in HepG2 cells. We found that usnic acid causes endoplasmic reticulum (ER) stress demonstrated by the increased expression of typical ER stress markers, including CHOP, ATF-4, p-eIF2alpha, and spliced XBP1. Usnic acid inhibited the secretion of Gaussia luciferase measured by an ER stress reporter assay. An ER stress inhibitor 4-phenylbutyrate attenuated usnic acid-induced apoptosis. Moreover, usnic acid significantly increased the cytosolic free Ca(2+) concentration. Usnic acid increased the expression of calcium release-activated calcium channel protein 1 (CRAM1 or ORAI1) and stromal interaction molecule 1, two key components of store-operated calcium entry (SOCE), which is the major Ca(2+) influx pathway in non-excitable cells, this finding was also confirmed in primary rat hepatocytes. Furthermore, knockdown of ORAI1 prevented ER stress and ATP depletion in response to usnic acid. In contrast, overexpression of ORAI1 increased ER stress and ATP depletion caused by usnic acid. Taken together, our results suggest that usnic acid disturbs calcium homeostasis, induces ER stress, and that usnic acid-induced cellular damage occurs at least partially via activation of the Ca(2+) channel of SOCE.

Gastroprotective and antioxidant effects of usnic acid on indomethacin-induced gastric ulcer in rats.[Pubmed:16169175]

J Ethnopharmacol. 2006 Jan 3;103(1):59-65.

Usnea longissima, a medicinal lichen of Anatolia (Turkey), is used in the treatment of gastric ulcer in local folk medicine. In this paper, the gastroprotective effect of usnic acid (UA) isolated from Usnea longissima was investigated in the indomethacin-induced gastric ulcers in rats at doses of 25, 50, 100 and 200 mg/kg body weight. The gastric lesions were significantly reduced by all doses of UA as compared with the indomethacin (25 mg/kg body weight) treated group. In the stomach tissues of treated animals, the in vivo antioxidant levels were evaluated. The administration of indomethacin caused a significant decrease in the levels of superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH), and an increase in the lipid peroxidation (LPO) level (p < 0.05). The administration of all doses of UA reversed the trend, inducing a significant increase of SOD, GSH and GPx levels and a reduction in LPO level in tissues. However, catalase (CAT), glutathione reductase (GR) and myeloperoxidase (MPx) activities, increased by indomethacin, were found to be lower in the UA- and ranitidine-treated groups. The gastric mucosal constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) activities were also investigated in tissues of UA- (100 mg/kg), ranitidine- (50 mg/kg) and indomethacin-treated rat groups. The administration of UA and ranitidine increased the cNOS activity and lowered the iNOS activity as compared with indomethacin-treated group. These results suggest that the gastroprotective effect of UA can be attributed to its reducing effect on the oxidative damage and neutrophil infiltration in tissues.

Acaricidal activity of usnic acid and sodium usnic acid against Psoroptes cuniculi in vitro.[Pubmed:24770718]

Parasitol Res. 2014 Jun;113(6):2387-90.

Usnic acid, a major active compound in lichens, was first isolated in 1884. Since then, usnic acid and its sodium salt (sodium usnic acid) have been used in medicine, perfumery, cosmetics, and other industries due to its extensive biological activities. However, its acaricidal activity has not been studied. In this paper, we investigated the acaricidal activity of usnic acid and sodium usnic acid against Psoroptes cuniculi in vitro. After evaluating the acaricidal activity and toxicity of usnic acid and sodium usnic acid in vitro, the results showed that at doses of 250, 125, and 62.5 mg/ml, usnic acid and sodium usnic acid can kill mites with 91.67, 85.00, and 55.00% and 100, 100, and 60.00% mortality after treatment 24 h. The LT50 values were 4.208, 8.249, and 16.950 h and 3.712, 7.339, and 15.773 h for usnic acid and sodium usnic acid, respectively. Sodium usnic acid has a higher acaricidal activity than usnic acid, which may be related to the difference in their structures.

Description

(+)-Usnic acid is isolated from isolated from lichens, binds at the ATP-binding pocket of mTOR, and inhibits mTORC1/2 activity. (+)-Usnic acid inhibits the phosphorylation of mTOR downstream effectors: Akt (Ser473), 4EBP1, S6K, induces autophay, with anti-cancer activity.

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