Table 2.
Pharmacological activities of Cassia obtusifolia extracts.
Pharmacological Activity | Part of Plant | Type of Extract | In Vivo/ In Vitro |
Model | Administration (In Vivo) | Dose Range | Active Concentration | Reference |
---|---|---|---|---|---|---|---|---|
Neuroprotective Activity | Seeds | 85% EtOH ext. | In vivo | Ameliorate scopolamine or 2VO-induced memory impairments by inhibiting AChE | Oral | 25–100 mg/kg | 50 mg/kg | [8] |
Seeds | 85% EtOH ext. | In vivo | Neuroprotection by inhibition of pro-inflammatory genes iNOX, and COX-2, and increased neurotrophic factor expression of pCREB and BDNF | Oral | 10, 50 mg/kg | 50 mg/kg | [33] | |
Seeds | 85% EtOH ext. | In vitro | Reduced Aβ toxicity and maintenance of Ca2+ dysregulation and excitotoxicity, mitochondrial dysfunction in primary hippocampal cultures | - | 0.1–10 µg/mL | 1, 10 µg/mL | [11] | |
Seeds | EtOH ex. | In vivo | protected the dopaminergic cells against 6-OHDA- and MPP+-induced neurotoxicities in primary mesencephalic cultures and in a mouse model in PD | Intraperitoneal injection | 0.1–10 µg/mL for DA, 50 mg/kg mouse | 0.1, 1 µg/mL 50 mg/kg |
[34] | |
Seeds | EtOH ext. | In vitro | Inhibited cell loss against 6-OHDA-induced DA neural toxicity by an anti-oxidant and anti-mitochondrial-mediated apoptosis mechanism in PC12 cells. | - | 0.1–10 µg/mL 1000 µg/mL for DPPH, ABTS |
1 µg/mL ROS, 10 µg/mL GSH, 75% Casp-3, 92%-DPPH, 85% ABTS | [35] | |
Seeds | MeOH ext. EtOAc fr. CH2Cl2 fr. BuOH fr. |
In vitro | Inhibitory activity against MAO-A, and MAO-B | - | 0.25–120 µg/mL | EtOAc fr. exhibited greatest inhibitory IC50 = 20, and 56 µg/mL activity against MAO-A, and MAO-B | [36] | |
Seeds | MeOH ext. EtOAc fr. CH2Cl2 fr. BuOH fr. H2O fr. |
In vitro | Inhibitory activity against AChE, BChE, BACE1 | - | 0.4–120 µg/mL | IC50 = 9.45~29 µg/mL for AChE, IC50 = 7.58~49 µg/mL for BChE, IC50 = 26~96 µg/mL for BACE1 | [10] | |
Seeds | 85% EtOH ext. | In vivo | Ameliorate Aβ-induced LTP impairment in the acute hippocampal slices and regulates GSK-3β, Akt signaling pathways through the inhibition of iNOS, COX expression | - | 1 and 10 µg/mL | 10 µg/mL | [35] | |
Hepatoprotective Activity | Seeds | MeOH ext. | In vitro | Protection against tacrine-induced hepatotoxicity in HepG2 cells | - | 300 µg/mL | 300 µg/mL | [36] |
Seeds | 70% EtOH ext. EtOAc, CH2Cl2, BuOH, H2O fr. |
In vitro | Protective effect against t-BHP-induced hepatotoxicity in HepG2 cells | - | 10–100 µg/mL | EtOAc fr. showed most potent hepatoprotective activity (30 µg/mL) | [12] | |
Seeds | EtOH ext. | In vivo | Hepatoprotective effects against CCl4-induced liver injury in mice | Intraperitoneal injection | 0.5, 1, 2 g/kg | Reduced ALT and AST, Ca2+, MDA, and increased GSH, SOD, GR, GPx, GST, CYP2E1 (2 g/kg) | [15] | |
seeds | EtOAc fr. CH2Cl2 fr. BuOH fr. H2O fr. |
In vitro | Protective effect against t-BHP-induced hepatotoxicity in HepG2 cells | - | 12.5–50 µg/mL | EtOAc fr. showed most potent hepatoprotective activity (50 µg/mL) | [37] | |
Seeds | 70% EtOH ext. | In vivo | (a) Significantly decreased the levels of AST, ALT, TG, TC, TNF-a, IL-6, IL-8 and MDA; (b) Increased the levels of SOD and GSH; (c) Significantly increased the mRNA expression levels of LDL-R | Oral | 0.5–2 g/kg | (a) Dose-dependently decreased biomarkers at 0.5–2 g/kg; (b) Dose-dependently decreased at 0.5–2 g/kg; (c) Significantly increased the levels of LDL-R at 2 g/kg | [38] | |
Anti-diabetic Activity | Seeds | MeOH ext. EtOAc fr. CH2Cl2 fr. BuOH fr. H2O fr. |
In vitro | Inhibitory activity against PTP1B and α-glucosidase | - | 0.4–400 µg/mL for PTP1B, 0.16–400 µg/mL for α-glucosidase |
MeOH ext. (IC50 = 14 µg/mL) and EtOAc fr. (IC50 = 74 µg/mL) exhibited greatest inhibitory activity against PTP1B and α-glucosidase | [9] |
Seeds | EtOH ext. | In vitro | Inhibitory activity against α-glucosidase | - | 1000 µg/mL | 20% inhibition of α-glucosidase (1000 µg/mL) | [39] | |
Anti-inflammatory, Antioxidant, and Immune-modulatory Activities | Roasted seeds | Hot H2O ext. | In vivo | Protection against dextran sulfate sodium (DSS)-induced colitis through the inhibition of (IL)-6, COX-2, NF-κB | Oral | 1 g/kg | Significantly reduced clinical signs and the levels of inflammatory mediators (at concentration 1 g/kg) | [40] |
Seeds | H2O soluble polysaccharide fr. | In vitro | Increased immune-modulatory activity by promoting phagocytosis and stimulating the production of NO and cytokines TNF- and IL-6 on macrophage cell line RAW264.7 | - | 62.5–500 µg/mL | Stimulates NO, TNF- and IL-6 expression (250 µg/mL) and promotes phagocytic activity (500 µg/mL) | [41] | |
Seeds | MeOH ext. | In vitro | DPPH, Fe [II], superoxide radicals scavenging activity and inhibit ß-carotene degradation | - | 1 mg/mL | Inhibition 65.79% DPPH, 50.78% superoxide radical, 49.92% inhibit ß-carotene degradation,1292 mM Fe [II] inhibited (at 1 mg/mL) | [14] | |
Antimicrobial Activity | Seeds | MeOH ext. Hexane fr. EtOAc fr. CH2Cl2 fr. BuOH fr.H2O fr. |
In vitro | Bifidobacterium adolescentis, B. bifidum, B. longum, B. breve, Clostridium perfringens, Escherichia coli, Lactobacillus casei | - | 5 mg discs−1 | CH2Cl2 fr, MeOH ext. and Hexane fr. exhibited the greatest antibacterial activity | [7] |
Leaf | Pet ether ext. EtOH ext. Chloroform ext. |
In vitro | Aspergilus fumigatus, Staphylococcus aureus, Enterococcus faecalis, E. coli, Klebsiella sp., Candia albicans | - | 0.6–1 mg/mL | Pet ether, chloroform ext. active against C. albicans (MIC 0.3524, and 0.4239 mg/mL), ethanol E. faecalis (MIC 0.2738 mg/mL) | [18] | |
stem | Pet ether ext. EtOH ext. Chloroform ext. |
In vitro | Aspergilus fumigatus, Staphylococcus aureus, Enterococcus faecalis, E. coli, Klebsiella sp., Candia albicans | 0.6–1 mg/mL | Ethanol, pet ether, chloroform ext. was more active against E.faecalis (MIC 0.298, 0.254, and 0.589 mg/mL, respectively) | [18] | ||
Whole plant | MeOH ext. | In vitro | E. coli, P. aeruginosa, Enterobacter aerogenes Providencia stuartii, K.pneumoniae, Enterobacter cloacae, S. aureus | - | 256 µg/mL | inhibition of S. aureus, E. coli, P. aeruginosa, E. aerogenes, K. pneumoniae (MIC ranges of 64–289 μg/mL | [42] | |
Larvicidal Activity | Seeds | MeOH ext. | In vitro | Larvicidal activity against Aedes aegypti and Culex pipiens pallens | - | 10–300 ppm | 40 ppm | [43] |
Seeds | Chloroform fr. | In vitro | Larvicidal activity against A. aegypti, Aedes togoi, and Cx. pipiens | - | 25 mg/L | 100% Mortality (at concentration 25 mg/L) | [44] | |
Leaf | EtOH ext. | In vitro | Larvicidal activity against Anopheles stephensi | - | 25–125 mg/L | LC50 = 52.2 mg/L, LC90 = 108.7 mg/L (at concentration 25 mg/L) | [45] | |
Leaf | EtOH ext. | In vitro | Anti-oviposition activity against Anopheles stephensi | - | 100–400 mg/L | 92.5% for 400 mg/L 87.2% for 300 mg/L 83.0% for 200 mg/L |
[45] |