Central analgesic activity of the aqueous and ethanolic extracts of the leaves of Albizia lebbeck: role of the GABAergic and serotonergic pathways
-
Girish G. Meshram
,
Anil Kumar
Abstract
Albizia lebbeck Benth. is extensively used in Indian traditional medicine for treating several painful and inflammatory disorders. The possible central analgesic activity and the underlying mechanism of action of the aqueous (AE) and ethanolic extracts (EE) of the leaves of A. lebbeck were investigated in Wistar rats using Eddy’s hot plate and the tail flick tests. In order to investigate the underlying mechanism of action, rats were pretreated with naloxone, bicuculline or methysergide and then were administered a per os (p.o.) dose of AE or EE. AE and EE caused a significant (p<0.05) elevation in the mean basal reaction time in the hot plate method and an increase in the latency time in the tail flick method. In rats pretreated with bicuculline and methysergide, a significant (p<0.05) reduction in the analgesic activity was observed in comparison to AE and EE. Thus, AE and EE exhibited significant central analgesic activity and act possibly via the GABAergic and serotonergic pathways. The flavonoids and saponins found in the leaves could be responsible for the observed effect.
1 Introduction
The major classes of drugs to alleviate pain are opioids and non-steroidal anti-inflammatory agents, but their undesirable side effects such as tolerance, dependence [1] and gastric irritation [2] have limited their use. There has hence been a drive amongst researchers to derive new medicinal products from plant constituents such as flavonoids, saponins, steroids, polyphenols, coumarins [3], terpenes, stearic acid and alkaloids [4]. These natural products may provide easy accessibility, cost benefits, and fewer side effects to patients.
Albizia lebbeck Benth., known as Sirisa in Sanskrit, is a tree commonly found in the Indian subcontinent. Various parts of the tree have been used for ages in traditional Indian medicine for treating several painful and inflammatory aliments. The bark is used for the treatment of asthma, bronchitis, arthritis, gingivitis, toothache, allergies, leukoderma, leprosy, snake bites, malaria, and fractures [5]. The leaves are claimed to be useful in night blindness and syphilis. The smell of the flowers is used to treat hemicranias [6]. The seeds are boiled and eaten by natives to treat gonorrhoea, diarrhoea and piles [7]. The seed oil is applied topically to treat leukoderma. The flowers and seeds are also claimed to have aphrodisiac properties [8].
The bark of A. lebbeck has been in the centre of attention due to its wide range of pharmacological activities such as antiinflammatory, analgesic, antiarthritic, antioxidant, antifertility, immunomodulatory, mast cell stabilising, antitumour and antimalarial activities in animal studies. There are clinical studies showing its use in asthma and allergic conjunctivitis [9]. The most abundant and accessible medicinal component of the tree, i.e., the leaves, has so far remained a silent bystander despite possessing pleiotropic properties such as anticonvulsive [10], nootropic [11], antiulcer [12] and antimicrobial [13] activities. There are no studies reporting the analgesic activity of the leaves till date.
Phytochemical studies on the leaves of A. lebbeck have revealed the presence of potentially bioactive alkaloids [14], flavonoids [15] and hexaglycosylated saponins [16]. The extracts of the leaves affected the brain levels of serotonin and γ-aminobutyric acid (GABA) [11], which are central mediators of pain. The absence of previous studies and the ability of the leaves to affect central neurotransmitters led us to undertake this study so as to evaluate the possible central analgesic activity and the underlying mechanism of action of the aqueous (AE) and the ethanolic extracts (EE) of the leaves of A. lebbeck in rats.
2 Material and methods
2.1 Ethical considerations
Experimental procedures and protocols used in this study were approved by the Institutional Animal Ethics Committee of the Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, and conform to the “Guidelines for care and use of animals in scientific research (Indian National Science Academy 1998, revised 2000).”
2.2 Plant material
The leaves were obtained from the botanical garden of Aligarh Muslim University (A.M.U.) Campus, Aligarh, India, in May 2011 and were authenticated by a botanist. A voucher specimen (voucher no.2149) is kept in the Department of Botany, A.M.U., for further reference. About 100 g of the powder prepared from shade-dried leaves was subjected to Soxhlet extraction for 16 h using 5 L of distilled water and 5 L of 99.9% ethanol (Scientific OEM, Mumbai, Maharashtra, India), respectively, as solvents. The semisolid, greenish-brown extracts obtained were dried under partial vacuum using a rotary evaporator.
The percentage yield based on the dried starting material for the AE was 21%, and that for the EE was 12.4%. The doses of 50, 100 and 200 mg/kg body weight (b.w.) of AE and EE were prepared by suspending the dried extracts in distilled water. The extracts were administered to the rats per os (p.o.).
2.3 Animals
Wistar rats (100–150 g) were obtained from the Animal House, Jawaharlal Nehru Medical College, Aligarh, India. They were housed at a temperature of 24±2 °C, 12-h light/day cycles, and 35%–60% humidity in polypropylene cages and fed with standard rodent diet with water ad libitum. Animals were deprived of food but not water 4 h before the experiment.
2.4 Drugs
Racemic pentazocine was procured from Ranbaxy Laboratories Limited (Mumbai, Maharashtra, India). Naloxone, bicuculline and methysergide were purchased from Sigma-Aldrich Corporation (Bangalore, Karnataka, India).
2.5 Hot plate method
The test was carried out according to the method described earlier [17]. The rats were divided into eight groups (n=6), each receiving distilled either water (control), 15 mg/kg b.w. intraperitoneal (i.p.) pentazocine (reference standard), or 50, 100 or 200 mg/kg b.w. p.o. of either AE or EE. They were placed on a hot plate maintained at a temperature of 56±0.5 °C. The latency to lick the hind paws or jump from the hot plate was taken as the reaction time. The reaction time was noted at 0, 15, 30, 45, 60, 75, 90, 120 and 180 min after drug administration. The cutoff time was considered as 15 s.
2.6 Tail flick method
The test was carried out according to the method described earlier [18]. The rats were divided into 8 groups (n=6), each receiving either distilled water (control), 15 mg/kg b.w. i.p. pentazocine (reference standard), or 50, 100 or 200 mg/kg b.w. p.o. of either AE or EE. The proximal third of the tail was placed 1.5 cm above a nichrome wire. The reaction time was considered as the time required by the rat to flick its tail. The intensity of the current was kept at 4 mA. If necessary, small adjustments of the current were made at the beginning of the experiment in order to obtain three consecutive baseline tail-flick latencies within 6 s. The reaction time was noted at 0, 15, 30, 45, 60, 75, 90, 120 and 180 min after drug administration. The cutoff time was considered as 15 s.
2.7 Pretreatment with receptor antagonists
In order to evaluate the neurotransmitter systems involved in the analgesic activity of A. lebbeck, rats were pretreated with 2 mg/kg b.w. i.p. naloxone (opioid receptor antagonist), 1 mg/kg b.w. i.p. bicuculline (GABA receptor antagonist) or 1 mg/kg b.w. i.p. methysergide (serotonin receptor antagonist). The drugs were injected immediately after evaluating the baseline response of the rats in either of the two tests, and 10 min before the administration of the 200 mg/kg b.w. p.o. dose of AE and EE, respectively.
2.8 Statistical analysis
Results are expressed as mean±SEM. Statistical analysis was performed using one-way analysis of variance (ANOVA) followed by multiple Tukey’s comparison test. A value of p<0.05 was considered statistically significant.
3 Results
3.1 Hot plate method
The AE and EE of A. lebbeck leaves at doses of 50, 100 and 200 mg/kg b.w. provoked a significant and dose-dependent increase in the mean basal reaction time in the hot plate test compared to the control group. The onset of action, for each of the doses of both AE and EE, was between 15 and 30 min, and its duration was up to 120 min. The highest inhibition by AE of nociception of the stimulus was observed as (4.9±0.09) s (p<0.05), (6.15±0.15) s (p<0.05) and (6.92±0.14) s (p<0.05) for the doses 50, 100 and 200 mg/kg b.w., respectively, at 75 min after its administration, while the values for EE were (4.97±0.06) s (p<0.05), (6.52±0.10) s (p<0.05) and (8.33±0.11) s (p<0.05) under the respective conditions (Table 1).
Analgesic effects of A. lebbeck extracts and reference drugs in the hot plate test.
| Group | Analgesic effect, s | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Before drug | 15 min | 30 min | 45 min | 60 min | 75 min | 90 min | 120 min | 180 min | |
| Distilled water | 3.00±0.12 | 3.22±0.05 | 3.07±0.04 | 3.17±0.021 | 3.08±0.04 | 3.17±0.056 | 3.10±0.06 | 3.07±0.03 | 3.02±0.02 |
| Pentazocine 15 mg/kg b.w. | 3.18±0.07 | 5.67±0.27a | 11.32±0.31a | 9.60±0.17a | 8.65±0.22a | 7.25±0.31a | 5.80±0.22a | 4.57±0.24a | 3.73±0.12a |
| AE 50 mg/kg b.w. | 3.10±0.04 | 3.20±0.10b | 3.75±0.08a,b | 4.35±0.09a,b | 4.53±0.07a,b | 4.90±0.09a,b | 4.23±0.11a,b | 3.77±0.09a,b | 3.18±0.07b |
| AE 100 mg/kg b.w. | 3.07±0.03 | 3.17±0.08b | 3.72±0.07a,b | 3.90±0.07a,b | 4.58±0.17a,b | 6.15±0.15a,b | 4.47±0.04a,b | 4.07±0.04a | 3.15±0.08b |
| AE 200 mg/kg b.w. | 3.03±0.03 | 3.05±0.03b | 3.48±0.06b | 4.20±0.14a,b | 5.63±0.08a,b | 6.92±0.14a | 6.32±0.10a,b | 4.30±0.11a | 3.1 5±0.08b |
| EE 50 mg/kg b.w. | 3.10±0.04 | 3.18±0.10b | 3.77±0.08a,b | 4.62±0.13a,b | 4.75±0.11a,b | 4.97±0.06a,b | 4.25±0.10a,b | 3.78±0.10a,b | 3.18±0.07b |
| EE 100 mg/kg b.w. | 3.07±0.03 | 3.15±0.08b | 3.73±0.07a,b | 3.90±0.07a,b | 4.52±0.15a,b | 6.52±0.10a,b | 4.48±0.04a,b | 4.08±0.05a | 3.15±0.08b |
| EE 200 mg/kg b.w. | 3.03±0.03 | 3.03±0.03b | 3.50±0.07a,b | 4.23±0.14a,b | 6.35±0.18a,b | 8.33±0.11a,b | 6.33±0.09a,b | 4.32±0.12a | 3.15±0.08b |
| AE 200 mg/kg b.w.+N | 3.05±0.02 | 3.07±0.06 | 3.43±0.06 | 4.22±0.06 | 5.73±0.08 | 6.33±0.22 | 6.10±0.13 | 4.77±0.20 | 3.27±0.08 |
| AE 200 mg/kg b.w.+B | 3.07±0.03 | 3.21±0.07 | 3.53±0.11 | 3.72±0.15 | 3.90±0.29c | 4.17±0.25c | 4.05±0.22c | 3.73±0.14 | 3.18±0.09 |
| AE 200 mg/kg b.w.+M | 3.03±0.04 | 3.18±0.07 | 3.30±0.07 | 4.00±0.32 | 4.92±0.20c | 6.10±0.12c | 5.12±0.16c | 4.28±0.16 | 3.20±0.17 |
| EE 200 mg/kg b.w.+N | 3.10±0.08 | 3.15±0.07 | 3.63±0.10 | 4.70±0.21 | 6.45±0.22 | 7.82±0.17 | 6.25±0.20 | 4.63±0.25 | 3.45±0.19 |
| EE 200 mg/kg b.w.+B | 3.07±0.06 | 3.12±0.06 | 3.50±0.15 | 4.00±0.22 | 4.53±0.15d | 5.85±0.28d | 4.75±0.22d | 4.20±0.14 | 3.37±0.09 |
| EE 200 mg/kg b.w.+M | 3.12±0.09 | 3.20±0.10 | 3.83±0.20 | 4.60±0.28 | 5.30±0.24d | 6.58±0.41d | 5.67±0.28 | 4.57±0.27 | 3.32±0.14 |
AE, aqueous extract of A. lebbeck leaves; EE, ethanolic extract of A. lebbeck leaves; N, naloxone 2 mg/kg b.w.; B, bicuculline 1 mg/kg b.w.; M, methysergide 1 mg/kg b.w. One-way ANOVA followed by multiple Tukey’s comparison test. Values are the mean±SEM, n=6 in each group. aindicates p<0.05, as compared to the control group. bindicates p<0.05, as compared to pentazocine 15 mg/kg b.w. group. cindicates p<0.05 as compared to AE 200 mg/kg b.w. group. dindicates p<0.05, as compared to the EE 200 mg/kg b.w. group.
3.2 Tail flick method
AE and EE at doses of 50, 100 and 200 mg/kg b.w. caused significant and dose-dependent increases in latency of the flick tail response. The onset of action, for each of the doses of AE and EE, was between 15 and 30 min, and it lasted until 120 min. The highest nociception inhibition of the stimulus by the AE was observed as (5.45±0.16) s (p<0.05), (6.03±0.21) s (p<0.05) and (6.22±0.13) s (p<0.05) for the doses 50, 100 and 200 mg/kg b.w., respectively, at 75 min after its administration, while the values for EE were (5.97±0.11) s (p<0.05), (6.52±0.08) s (p<0.05) and (7.3±0.08) s (p<0.05) under the respective conditions (Table 2).
Analgesic effects of A. lebbeck extracts and reference drugs in the tail flick test.
| Group | Analgesic effect, s | ||||||||
|---|---|---|---|---|---|---|---|---|---|
| Before drug | 15 min | 30 min | 45 min | 60 min | 75 min | 90 min | 120 min | 180 min | |
| Distilled water | 3.40±0.05 | 3.40±0.04 | 3.40±0.07 | 3.42±0.05 | 3.52±0.02 | 3.40±0.05 | 3.37±0.05 | 3.50±0.11 | 3.52±0.10 |
| Pentazocine 15 mg/kg b.w. | 3.32±0.04 | 4.30±0.19a | 8.03±0.27a,b | 8.78±0.11a,b | 7.50±0.22a | 6.55±0.15a | 5.32±0.37a | 4.23±0.18a | 3.38±0.09 |
| AE 50 mg/kg b.w. | 3.52±0.05 | 4.20±0.14a | 4.50±0.12a,b | 4.92±0.17a,b | 5.15±0.18a,b | 5.45±0.16a,b | 4.70±0.04a | 4.50±0.03a | 3.88±0.09 |
| AE 100 mg/kg b.w. | 3.37±0.02 | 4.35±0.21a | 4.68±0.19a,b | 4.72±0.18a,b | 5.20±0.03a,b | 6.03±0.21a | 4.70±0.12a | 4.70±0.05a | 3.81±0.20 |
| AE 200 mg/kg b.w. | 3.50±0.03 | 4.00±0.04 | 4.72±0.03a,b | 5.00±0.07a,b | 5.23±0.11a,b | 6.22±0.13a | 4.92±0.04a | 4.50±0.10a | 3.52±0.09 |
| EE 50 mg/kg b.w. | 3.53±0.02 | 4.03±0.03a | 4.98±0.29a,b | 5.37±0.18a,b | 5.91±0.43a,b | 5.97±0.11a,b | 5.20±0.13a | 4.70±0.10a | 3.58±0.12 |
| EE 100 mg/kg b.w. | 3.52±0.07 | 4.12±0.08a | 4.95±0.14a,b | 5.62±0.20a,b | 6.08±0.08a,b | 6.52±0.02a | 5.83±0.11a | 4.70±0.12a | 3.97±0.23 |
| EE 200 mg/kg b.w. | 3.48±0.03 | 3.68±0.10 | 4.33±0.17a,b | 5.00±0.13a,b | 6.33±0.21a,b | 7.30±0.08a,b | 6.30±0.16a,b | 4.92±0.15a,b | 3.75±0.11 |
| AE 200 mg/kg b.w.+N | 3.52±0.11 | 4.24±0.25 | 5.16±0.29 | 5.34±0.25 | 5.82±0.29 | 6.54±0.12 | 5.46±0.29 | 4.64±0.25 | 3.72±0.17 |
| AE 200 mg/kg b.w.+B | 3.40±0.11 | 3.97±0.15 | 4.42±0.18 | 4.55±0.13 | 4.50±0.12c | 5.05±0.10c | 4.22±0.10c | 4.30±0.14 | 3.70±0.13 |
| AE 200 mg/kg b.w.+M | 3.37±0.09 | 4.03±0.15 | 4.35±0.13 | 4.65±0.11 | 5.00±0.11 | 5.67±0.16c | 4.27±0.18c | 4.10±0.06 | 3.57±0.16 |
| EE 200 mg/kg b.w.+N | 3.40±0.10 | 3.57±0.08b | 4.30±0.19 | 4.98±0.17 | 6.45±0.16 | 7.50±0.22 | 6.62±0.20 | 4.67±0.17 | 3.67±0.25 |
| EE 200 mg/kg b.w.+B | 3.43±0.15 | 3.58±0.05 | 4.17±0.12 | 4.55±0.13 | 4.98±0.20d | 5.53±0.19d | 4.88±0.16d | 4.47±0.17 | 3.58±0.16 |
| EE 200 mg/kg b.w.+M | 3.42±0.12 | 3.67±0.09 | 4.50±0.18 | 5.17±0.30 | 5.43±0.30d | 6.48±.018d | 5.55±0.26 | 4.52±0.13 | 3.68±0.26 |
AE, aqueous extract of A. lebbeck leaves; EE, ethanolic extract of A. lebbeck leaves; N, naloxone 2 mg/kg b.w.; B, bicuculline 1 mg/kg b.w.; M, methysergide 1 mg/kg b.w. One-way ANOVA followed by multiple Tukey’s comparison test. Values are the mean±SEM, n=6 in each group. aindicates p<0.05, as compared to the control group. bindicates p<0.05, as compared to pentazocine 15 mg/kg b.w. group. cindicates p<0.05 as compared to AE 200 mg/kg b.w. group. dindicates p<0.05, as compared to the EE 200 mg/kg b.w. group.
3.3 Comparison with pentazocine
The analgesic activity of 15 mg/kg b.w. i.p. pentazocine was superior to all doses of AE and EE in both Eddy’s hot plate and the tail flick tests in the time period of 15–60 min following drug administration. The 200 mg/kg b.w. dose of EE showed a significantly higher response to pentazocine in the time period of 75–120 min after drug administration in both tests employed, while the 200 mg/kg b.w. dose of AE showed a significantly superior response to that of pentazocine in the time period of 75–120 min after drug administration only in the hot plate test but not in the tail flick test (Tables 1 and 2).
3.4 Pretreatment with receptor antagonists
Pretreatment with 2 mg/kg b.w. i.p. naloxone did not cause any significant reduction in the analgesic activity of the 200 mg/kg b.w. dose of AE and EE in both tests, while pretreatment with 1 mg/kg b.w. i.p. of either bicuculline or methysergide significantly decreased the analgesic activity of the same dose of AE and EE between 60 and 90 (bicuculline) or 75 (methysergide) min after drug administration. The reduction in the analgesic activity of AE and EE was higher upon pretreatment with bicuculline than with methysergide (Tables 1 and 2).
4 Discussion and conclusion
The extracts of the leaves of A. lebbeck did not produce toxic effects or behavioural changes in rats at doses of up to 2000 mg/kg b.w. p.o.; hence, doses of 50, 100 and 200 mg/kg b.w. p.o. were selected for the present study [12].
The Eddy’s hot plate test is useful for the evaluation of centrally acting analgesics which elevate the pain threshold of animals towards heat [19]. It is thought to be responsive to opioids and measures the complex response to a non-inflammatory, acute nociceptive stimulus [20]. The responses of jumping, withdrawal of the paws and licking of the paws are thus delayed. The AE and EE showed significant analgesic activity at doses of 50, 100 and 200 mg/kg b.w.
In the tail flick test, the simple tail flick which is the endpoint of this test is mediated as a spinal reflex. This escape reaction can be regarded as a complex phenomenon mediated by the brain. Therefore, the observation of the escape reaction can be regarded as an assessment of the influence of the drug on the brain [21]. The AE and EE of the leaves of A. lebbeck caused significant delays in the reaction times at the doses of 50, 100 and 200 mg/kg b.w.
Previous studies have reported the analgesic activity of the bark of A. lebbeck [22]. The reaction time in the tail flick test was prolonged from (4.50±0.15) s to (7.27±0.30) s by a dose of 400 mg/kg b.w. of the aqueous bark extract. In the present study, the reaction time was prolonged from (3.50±0.03) s to (6.22±0.13) s by a dose of 200 mg AE /kg b.w., suggesting that the analgesic activity of the leaves is comparable to that of the bark of A. lebbeck.
The analgesia produced by AE and EE is moderate, unlike the strong analgesia produced by pentazocine. However, the 200 mg/kg b.w. doses of AE and EE caused a significantly (p<0.05) higher analgesic activity compared to that of pentazocine at 15 mg/kg b.w. in the time period of 75 min–120 min. This could be due to the different pharmacokinetics of pentazocine which showed a maximal response at 45 min after its administration and then a gradual decline in both tests. The analgesic activity of AE and EE peaked at 75 min following their administration and then gradually declined.
The central analgesic activity of the leaves of A. lebbeck is probably mediated by the GABAergic and serotonergic pathways. This conclusion is based on the observation that the GABA receptor antagonist (bicuculline) and the serotonin receptor antagonist (methysergide) significantly reduced the analgesic effects in both tests.
Previous studies on the n-butanolic fractions of the leaves of A. lebbeck reported a decrease in the brain GABA concentration and an increase in the brain serotonin concentration at the dose of 10–25 mg/kg b.w. in mice. The brain GABA level increased and the brain serotonin level decreased at the higher dose of 50 mg/kg b.w. [11, 23]. The methanolic fraction of the chloroform soluble part of the EE of the leaves of A.lebbeck raised brain GABA and serotonin levels [10]. GABA and serotonin are two key neurotransmitters in the pain pathway. GABA is released by spinal cord interneurons and inhibits transmitter release by primary afferent terminals in the dorsal horn. Serotonin is the transmitter of inhibitory neurons running from the nucleus raphe magnus to the dorsal horn [24]. The role of GABA agonists and serotonin-noradrenaline reuptake inhibitors as analgesics is well established in the therapy of pain [25]. Hence, this interplay between the GABAergic and serotonergic pathways in the brain is suggested as the possible mechanism for the central analgesic activity of the leaves of A. lebbeck, which should be further examined by measuring GABA and serotonin levels.
The preliminary phytochemical screening of the AE and EE of the leaves of A. lebbeck revealed the presence of alkaloids, tannins, flavonoids and saponins [26]. The flavonoids were kaempferol 3-O-α-rhamnopyranosyl-(1→6)-p-glucopyranosyl(1→6)-0-galactopyranoside and quercetin 3-O-α-rhamnopyranosyl(1→6)-β-glucopyranosyl(1→6)-β-galactopyranoside [15]. The saponins were hexaglycosylated hexosides, i.e., albiziahexoside, albiziatrioside A [16]. High-performance thin-layer liquid chromatography studies of leaf extracts allowed the separation of up to 21 alkaloids, but their structures were not identified [14, 26]. Flavonoids and saponis are known to exhibit a diverse range of pharmacological activities such as antimicrobial, antiviral, antiplatelet, antioxidant, anticancer, antidiabetic, anti-inflammatory and analgesic effects [27, 28] through several mechanisms [29, 30]. Thus, the analgesic activity of A. lebbeck could be correlated to its flavonoids and saponins; however, the involvement of other secondary metabolites present in the leaves cannot be ruled out. The exact mechanism and the bioactive principles responsible for these actions remain to be elucidated.
In conclusion, the AE and the EE of the leaves of A. lebbeck possess central analgesic activity and possibly act via the GABAergic and serotonergic pathways, which is a step forward in exploring the complete medicinal potential of the leaves.
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©2015 by De Gruyter
Articles in the same Issue
- Frontmatter
- Larvicidal activity of the essential oil of Youngia japonica aerial parts and its constituents against Aedes albopictus
- Antiviral and antitumor activities of the lectin extracted from Aspidistra elatior
- Susceptibility of Microsporum canis arthrospores to a mixture of chemically defined essential oils: a perspective for environmental decontamination
- Central analgesic activity of the aqueous and ethanolic extracts of the leaves of Albizia lebbeck: role of the GABAergic and serotonergic pathways
- Three further triterpenoid saponins from Gleditsia caspica fruits and protective effect of the total saponin fraction on cyclophosphamide-induced genotoxicity in mice
- Acylated flavonol diglucosides from Ammania auriculata
- Synthesis and antimicrobial properties of N-substituted derivatives of (E)-2′,3″-thiazachalcones
Articles in the same Issue
- Frontmatter
- Larvicidal activity of the essential oil of Youngia japonica aerial parts and its constituents against Aedes albopictus
- Antiviral and antitumor activities of the lectin extracted from Aspidistra elatior
- Susceptibility of Microsporum canis arthrospores to a mixture of chemically defined essential oils: a perspective for environmental decontamination
- Central analgesic activity of the aqueous and ethanolic extracts of the leaves of Albizia lebbeck: role of the GABAergic and serotonergic pathways
- Three further triterpenoid saponins from Gleditsia caspica fruits and protective effect of the total saponin fraction on cyclophosphamide-induced genotoxicity in mice
- Acylated flavonol diglucosides from Ammania auriculata
- Synthesis and antimicrobial properties of N-substituted derivatives of (E)-2′,3″-thiazachalcones
