Oroxylum indicum, Sonapatha is traditionally used to treat asthma, biliousness, bronchitis, diarrhea, dysentery, fevers, vomiting, inflammation, leukoderma, skin diseases, rheumatoid arthritis, wound injury, and deworm intestine.
|Plant Part||Activity Type||Reference|
|Root/root bark, stem/stem bark, leaf, fruit||Hydroxyl, nitric oxide, superoxide, DPPH radical scavenging|||
|Leaf||DPPH, nitric oxide, superoxide, hydroxyl radical scavenging, reducing power|||
|Stem Bark||DPPH, nitric oxide, superoxide, hydroxyl radical scavenging, reducing power|||
The gastroprotective activity of 100 and 300 mg/kg b. wt. of 50% hydroalcoholic, petroleum ether, chloroform, ethyl acetate, and n-butanol extracts of root bark of Sonapatha were studied against ethanol-induced gastric damage. All extracts at a dose of 300 mg/kg showed a significant reduction in the ulcer index. The petroleum ether, n-butanol, and chloroform extracts were most effective when compared to ethyl acetate and hydroalcoholic root extracts. Likewise, these extracts of Sonapatha also reduced LOO and increased the activities of SOD, and catalase, and GSH levels, especially at a dose of 300 mg/kg in Wistar rats . Treatment of 100 and 250 mg/kg of hexane and acetone stem bark extracts of Sonapatha had a mild to moderate protective effect against different models of gastric ulcerations. The isolated chrysin and compound 1 from the stem bark of Sonapatha were superior gastroprotective agents in pylorus ligation and cold restrain-induced ulceritis models in rats . The butanol, petroleum ether, and ethanol extracts of stem bark of Sonapatha reduced the ethanol-induced gastric ulcers with an inhibitory index of 0.07±0.007 (99%), 0.27±0.011 (96%), and 0.87±0.044 (86%), respectively .
The cardioprotective effect of 70% methanol extract of root bark of Sonapatha was studied in doxorubicin-treated Sprague Dawley rats. The oral administration of animals with 200 and 400 mg/kg b. wt. Sonapatha extract for 14 days protected rats against doxorubicin-induced cardiotoxicity. The methanol extract of Sonapatha led to normalization of Electrocardiogram (ECG), ST-segment depression, and QRS complex in the hearts of doxorubicin treated rats. The serum marker enzymes like creatinine phosphokinase (CPK), AST, and LDH were significantly reduced by methanol extract of Sonapatha. The assessment of LOO, GSH, glutathione peroxidase, (GPx), and SOD in the heart tissue revealed a significant decline in LOO and rise in the GSH, GPx, and SOD levels in the Sonapatha treated group when compared to doxorubicin treatment alone. Histopathologic evaluation revealed focal degeneration, fragmentation, disorganization of myofibrils, and necrotic changes in the heart tissue after doxorubicin treatment whereas Sonapatha extract administration reduced these changes .
Administration of 300 and 500 mg/kg b. wt. of aqueous and ethanol extracts of Sonapatha for 21 days significantly reduced serum glucose levels in alloxan and dexamethasone-induced diabetes in Wistar rats . Methanol extract of the heartwood of Sonapatha reduced the activity of α-glucosidase (GAA; an enzyme involved in carbohydrate digestion and glycoprotein biosynthesis, which is highly activated in diabetes) indicating its antidiabetic potential . Similarly, hydroalcoholic extract (50% ethanol) of Sonapatha inhibited GAA activity in vitro. Sonapatha extract has been found to improve insulin sensitivity in cultured 3T3-L1 mature adipocytes. Oral administration of 250 mg/kg b. wt. of 50% ethanol extract of Sonapatha has reduced fasting blood glucose, low-density lipoprotein (LDL), and glycosylated hemoglobin (HbA1c) levels and elevated high-density lipoprotein (HDL) in streptozotocin-induced diabetic rat serum after 28 days post-treatment. Homeostasis model assessment-insulin resistance (HOMA-IR) index and quantitative insulin sensitivity check index (QUICKI) were also significantly reduced in Sonapatha treated diabetic rats after 28 days post-treatment . The seeds of Sonapatha extracted in 90% ethanol inhibited the rat intestinal GAA activity. The administration of 50 and 250 mg/kg b. wt. of alcoholic seed extract of Sonapatha non-significantly reduced the fasting glucose level in alloxan-induced diabetic mice however, its combination with acarbose significantly reduced the fasting glucose level . Similarly, 90% ethanol seed extract of Sonapatha at a dose of 50 and 200 mg/kg b. wt. in conjunction with acarbose inhibited glucose level in streptozotocin-induced diabetic mice significantly. The Sonapatha seed extract increased the antioxidative capacity by elevating GSH, SOD, and HDL followed by reduced LOO and LDL levels in prediabetic mice . The administration of 300 mg/kg b. wt. of aqueous and methanol extracts of Sonapatha leaves reduced the glucose, total cholesterol, triglyceride, protein, urea, and creatinine levels in alloxan-induced diabetic rats . Administration of 200 and 400 mg/kg b. wt. of 50% ethanol seed extract of Sonapatha for 21 days reduced serum glucose, triglyceride, and cholesterol levels in the glibenclamide-induced diabetic rats .
Obesity is one of the major health problems in humans and 13% of the adult world population is clinically obese. Obesity is associated with cardiovascular diseases, type II diabetes and certain cancers and Sonapatha has shown promise to reduce obesity preclinically. The 3T3-L1 adipocytes treated with hexanes, dichloromethane, ethyl acetate and methanol extracts of Sonapatha bark inhibited the lipid accumulation and lipase activity and the ethyl acetate extract was most effective . Similarly, 3T3-L1 adipocytes exposed to 50, 100, 150 or 200 μg/mL of 95% Sonapatha ethanol fruit extract for 2 and 10 days suppressed the accumulation of lipids and lipase activity in 3T3-L1 adipocytes concentration-dependently. Sonapatha fruit extract also reduced lipids, lipid esters, nucleic acids, glycogen and carbohydrates in 3T3-L1 adipocytes . The treatment of 3T3-L1 preadipocytes with 50, 100, 150 or 200 μg/mL fruit extract of Sonapatha inhibited lipid accumulation and the greatest effect was observed for 200 μg/mL. The study of mRNA expression showed that 200 μg/mL fruit extract suppressed the expression of fatty acid synthetase (FAS), sterol regulatory element-binding proteins 1c (SREBP-1c), proliferator-activated receptor-γ2 (PPARγ2), glucose transporter (GLUT4), and leptin in adipocytes indicating its potential as an antiobesity agent .
The aqueous and methanol extracts of Sonapatha stem bark induced apoptosis in MDA-MB-435S (human breast carcinoma), Hep3B (human hepatic carcinoma), and PC-3 (human prostate cancer) cells . The exposure of HeLa cells to 50, 100, 200, 250 and 500 petroleum ether, dichlromethane and methanol extracts of Sonapatha stem bark caused a concentration-dependent rise in the cytotoxic effect with an IC50 of 112.3±4.4, 171.7 ± 7.4 and 315.7 ± 6.5 μg/ml for petroleum ether, dichlromethane and methanol extracts, respectively. The petroleum ether extract was most cytotoxic and induced apoptosis indicated by membrane blebbing, nuclear fragmentation and apoptotic bodies and DNA fragmentation . The petroleum and chloroform stem bark extract of Sonapatha has been reported to exert dose-dependent cytotoxicity in MDA-MB-231 and MCF-7 breast cancer cells by XTT assay and also induced apoptosis indicated by DNA fragmentation measured by ELISA . The Sonapatha leaves extracted in methanol have shown the cytotoxic effect on HeLa cells with an IC50 of 3.87 μg/ml, whereas it did not exert any cytotoxicity on normal Vero and MDCK cells. The methanol leaf extract of Sonapatha induced apoptosis, which was characterized by nuclear fragmentation, condensation, and apoptotic bodies. The apoptosis induction by methanol extract was further characterized by FITC-Annexin V and propidium iodide assay by flow cytometry analysis. The flow cytometric evaluation has revealed the collection of cells in the G1/S phase of the cell cycle by increasing p53 expression . The cytotoxic effects of ethanol extract of wild Sonapatha and twigs cultured in vitro have triggered dose-dependent cytotoxicity in SiHa and HepG2 cells with IC50 of 440 and 480 µg mL-1, respectively for wild samples. However, the cytotoxicity was lower in the case of in vitro samples that exhibited the IC50 of 530 and 550 µg ml-1 for SiHa and HepG2 cells, respectively . The root bark of Sonapatha extracted in chloroform, ethyl acetate and n-butanol showed lethality in the brine shrimp assay and it was also cytotoxic to MCF-7 cells . The leaf, bark, pod, and seeds of Sonapatha extracted in ethanol showed a concentration-dependent increase in cytotoxicity by sulforhodamine B and clonogenic assays with the IC50 of 161.2±8.63, 286.73±33.01, 149.03±8.81, and 107.06±5.66 μg/mL for leaf, bark, pod, and seed extracts, respectively. The seed extract was most cytotoxic as indicated by colony-forming assay . The leaves and fruit of Sonapatha extracted in ethanol were cytotoxic to MCF-7 cells in sulforhodamine B and clonogenic assays having an IC50 of 57.02 ± 2.85 µg/mL and 131.3 ± 19.2 µg/mL, respectively. The leaf extract also inhibited cell migration, activated caspase 3, and triggered apoptosis and suppressed the expression of MMP 9, ICAMP1, and Rac1 genes in MCF-7 cells. RhoA was significantly elevated by both leaf and fruit extracts in MCF-7 cells . The methanol extract of Sonapatha leaves triggered cytotoxicity in a concentration-dependent manner with an IC50 of 6.25±1.06 µg/mL. The cytotoxic effect of Sonapatha seems to be mediated by the downmodulation of HPV18 oncoproteins E6 and E7, followed by the activation of caspase-8 and caspase-3 and higher mRNA expressions of p53, pRb, Fas, and FasL in HeLa cells. The Sonapatha methanol leaf extract increased IL-12 and reduced the IL-6 production in HeLa cells .
The root bark of Sonapatha extracted in methanol has been reported to heal partial burn wounds in mice receiving the topical application of 1 and 2.5% extract containing ointment. This was evident by higher wound contraction and reduced wound healing time. The histological evaluation revealed a time-dependent progression in the formation of dermis and reepithelialization. The methanol extract of Sonapatha also increased collagen synthesis and 2.5% extract was superior to 1% . Topical application of 5, 10, 20, and 30 % ethanol stem bark extract of Sonapatha increased wound contraction and reduced the mean wound healing time in a dose-dependent manner of the full thickness excision wounds of mice. The 10% extract was most effective as it produced the highest wound contraction and reduced healing time maximally. The biochemical analysis of collagen and DNA syntheses showed a dose-dependent rise, accompanied by a decline in the LOO. The Western blot analysis showed that infliction of excision wound upregulated NF-κB and COX-2, whereas topical application of Sonapatha ethanol extract reduced their expression .
Coronavirus disease 2019 (COVID-19) is an infectious disease caused by coronavirus-2 (SARS-CoV-2). Covid-19 became a pandemic at the beginning of 2020 and since then several deaths have occurred worldwide. Covid-19 infection is characterized by a severe life-threatening acute respiratory syndrome caused by hyperinflammatory response, vascular damage, microangiopathy, angiogenesis and widespread thrombosis. Currently, no specific treatment is available against COVID19 infection . The COVID-19 entry into the primary host-cell is mediated by specific binding of coronavirus spike proteins (s) to the angiotensin-converting enzyme II (ACE2) receptors of human organs. Therefore, blocking of ACE2 can reduce COVID-19 entry into the cell. The molecular docking and the surface plasmon resonance studies have shown that oroxylin A present in Sonapatha can suppress the entry of the SARS-CoV-2-spiked pseudotyped virus into ACE2 cells, as it binds well to the ACE2 (blocking its availability for COVID-19) receptors as shown by surface plasmon resonance and cell membrane chromatography . The 200 mg/kg baicalein another constituent of Sonapatha has been found to inhibit the replication of the COVID-19 virus and loss of body weight and reduce lung damage in hACE2 transgenic mice infected with SARS-CoV-2 and it also reduced SARS-CoV-2-induced injury in cultured Vero cells . Baicalein inhibited the replication of SARS-CoV-2 in vitro with an IC50 of 10 μM in Vero E6 cells by reducing oxygen consumption rate, oxidative phosphorylation and mitochondrial membrane potential . Molecular docking studies against the SARS-CoV-2 virus replication enzyme main protease (Mpro) revealed that four (baicalein-7-O-diglucoside, chrysin-7-O-glucuronide, oroxindin and scutellarein) of the eighteen constituents of Sonapatha had the potential to inhibit the activity of this enzyme and restrain COVID-19 infection .