INTRODUCTION:

Pterostilbene (PTB) a dimethylated analogue of resveratrol is a natural phytoalexin. It was isolated for the first time from Pterocarpus santalinus by Spath and Schlager.^1-3 It is present in the wood of various Pterocarpus species and in various Vaccinium berries. It has comparable antioxidant and anti-tumor effect as that of resveratrol. But PTB have higher bioavailability with better metabolic stability. As it is methoxyled at the 3 and 5 positions, is more lipophilic, increasing its intestinal absorption.⁴ The doses up to 250mg/day are safe to use as per human clinical trials.⁵

Pharmacological Actions Of PTB:

This section describes pharmacological activities exhibited by PTB except neuroprotective and antidiabetic activities which are reviewed earlier.

Anticancer activity:

PTB is effective against a various types of cancer. It may have a good prospect in the future clinic applications.⁶

PTB was found to be effective in cancer cell lines namely BC-l (human breast cancer), HT-1080 (human fibrosarcoma), LU-1 (human lung cancer), MEL-2 (human melanoma), COL-1 (human colon cancer), KB (human oral epidermoid carcinoma), KB-Vl (vinblastine resistant KB), P388 (murine lymphoid neoplasm), A-431 (human epidermoid carcinoma), LNCaP (hormone dependent human prostatic cancer), ZR-75-1 (hormone-dependent breast cancer) and U-373 (human glioblastoma).⁷PTB has been documented to show anticancer activity in all the stages of carcinogenesis. In the initial stage, normal cells start transforming into the cancerous cells as a result of irreversible genetic mutations exposure to oxidative stress, carcinogens and inﬂammatory injury.⁸ Extensive research regarding PTB in several In vitro and In vivo has revealed its several mechanistic approaches by which it produces antineoplastic effect such as activation of the nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) pathway, enhancement of interaction between Nrf2 and Kelch-like ECH-associated protein 1 (Keap1), a repressor protein that binds to Nrf2, inhibition of ROS production, enhanced antioxidant levels such as superoxide dismutase (SOD), CAT, GPx, HO-1, and NQO1 levels.^9-11 PTB has also exhibited the ability to reduce the risk of mutagenesis and cancer by producing inhibitory activity towards enzymes of cytochrome P450 family such as CYP1A1, CYP1A2, CYP2C8, CYP1B as well as UGT1A6 involved in pathogenesis of cancer. Thus, PTB demonstrated its beneficial effects in inhibiting initial stage of carcinogenesis.^12-14

In the stage of tumor promotion, chronic inﬂammation and oxidative stress transform cancerous cells to malignant cells with abnormal cell proliferation by evading immune surveillance and apoptosis having critical role in maintenance of normal cellular multiplication.^15-17 In this stage PTB is found to increase Fas and Fas ligand expression which is responsible for triggering death receptor ligation pathway of cancer cell apoptosis. PTB also acts by inducing exogenous apoptosis of cancer cells by altering the expression of the death receptors i.e., by reducing DcR-1/2 expression and increasing DR4/5 leading to activation of apoptosis caspase 3/7/8 as per a study^.18-20 PTB has also been proven for its ability to increase the expression of pro-apoptotic factors such as Bid, Bad, Bak and Bax and decrease the antiapoptotic factors such as Mcl-1, Bcl-xl and Bcl-2 and thus inducing apoptotic pathway. Several investigations have also proved that PTB also increases endoplasmic reticulum (ER) stress by increasing the expressions of C/EBP homologous protein (CHOP), phospho-PKR-like ER kinase (p-PERK) and activating transcription factor 4(ATF4) leading to reduction of calcium ions in ER thus enhancing cytoplasm-induced apoptotic activity in cancerous cells. Overall findings suggest that PTB produces cancerous cell death by triggering and enhancing apoptosis showing its potential as a potent anticancer agent.^21-23

Apart from this, various studies have proven that PTB triggers autophagy along with apoptosis in cancerous cells in thus playing a pro-death role. It is one of the promising anticancer strategies which acts by inhibiting tumor growth and malignant transformation and by inducing programmed cell death.²³ There are various studies which have exhibited several mechanisms through which PTB induce autophagy. PTB produces cell cycle arrest in S phase in cholangiocarcinoma cells, MCF-7 and Bcap-37 breast cancer cells, SAS and OECM-1 human oral cancer cells by inducing autophagy through downregulation of p62, p38, ERK1/2 and Akt and expression resulting into increased expression of autophagy related protein 5 (ATG5), endogenous Beclin-1, JNK1/2, LC3-I and microtubule-associated protein 1A/1B-light chain 3-II (LC3-II).^24-27 It has also been documented that PTB arrested cell proliferation in prostate carcinoma cell lines 22 Rv1 and DU145 by reducing the expression of tumor suppressor genes miR-106a/b, miR-21a and miR-17 leading to restoration of phosphatase and tensin homologue (PTEN) levels involved in cell cycle control through many pathways. It also decreased tumor development through the decrease in circulating levels of miR-106a-5p and miR-17- 5p and reverting PTEN level to normal in xenograft model.²⁸ PTB also produced downregulation of PI3K/Akt/mTOR signaling pathway controlled by PTEN, thus inducing apoptosis in Granta- 519 and JeKo-1 cell lines of mantle cell lymphoma and cell cycle inhibition at G0/G1 phase.^29,30 Apart from this PTB also caused reduction in urethane-induced lung tumor growth through the inactivation of EGFR/PI3K/Akt/ERK/mTOR pathway. PTB also induced G1 arrest, upregulation of several repair response proteins such as p16, p27, p21 and p53 and cell-intrinsic checkpoint and causes downregulation of cyclin-dependent kinase levels of Cdk6, Cdk4, cyclin E, Cdk2 and cyclin A responsible for Rb phosphorylation in HL-60 gastric cancer cell lines. Similarly, in H520 lung squamous cancer cell lines PTB caused S phase accumulation through upregulation of p27 and p21 expression and downregulation of cyclin E and cyclin A.³¹ Furthermore, PTB has also lead to activation of check point kinases 1/2 (CHK1/2), ataxia telangiectasia mutated (ATM) pathways p53 expression inhibiting proliferation of A549 and NSCLC lung cancer cell lines.²² Similarly in another study, PTB caused reduction in levels of CDK2, cdc25A and cyclin A2 as well as increase in levels of Chk2-induced accumulation of lymphoma cells in the S-phase.³³ Overall findings proved the potency of PTB to inhibit cancer promotion and progression through cell cycle arrest by several pathways.

In progression stage of cancer wherein malignant cells attack surrounding tissues and distant organs leading to metastasis, PTB has shown its efficacy to curb the invasion and metastasis of cancer and inhibit angiogenesis through upregulation and downregulation of several pathways.³⁴ These mechanisms included decreased production of positive regulatory factor VEGF in SK-MEL-2 human melanoma cell lines, suppression of Wnt/β –catenin signaling and AOM-induced GSK3 β phosphorylation and inhibition of VEGF in ICR mice, decrease in angiogenesis by reduction of MTA1-associated proangiogenic factors VEGF, HIF-1 α and IL-1 β in PC3M prostate carcinoma cells.³⁵ In a study, MTA1 inhibition by PTB caused decreased lymhangiogenesis and hemangiogenesis as shown through by VEGF-C, IL-1 β and CD31 immunoblot and immunostaining analyses in Pten +/f prostate-specific heterozygous mice.^36,37 Additionally, PTB has shown angiogenesis inhibition inactivation of c-Met responsible for metastasis, thus inhibiting perivascular migration, angiogenesis and invasion through CXCL1-mediated CXCR1 signaling and IL-8 in 231BrM breast cancer cells.³⁸ In an investigation, PTB caused reduction tumor metastasis induced by invadopodium formation through suppression of by expression of several microenvironmental factors such as cortactin, c-Src, Twist1, PDGFR- α, metalloproteinases MT1-MMP, MMP-2 and Tks5 in MDA-MB-231 human breast carcinoma cells.³⁹ In TPA-mediated HepG 2 cell line metastasis PTB caused inhibition of metastasis through downregulation of VEGF, EGF and PKC as well as through suppression of AP-1 and NFκ B activity, PI3K/AKT and MAPK phosphorylation pathways and MMP-9 gene expression.⁴⁰ Similarly, PTB exhibited its efficacy against oral cancer invasion and migration by inhibiting SP-1, NFκB and CREB expression as well as DNA-binding action on u-PA and MMP-2 promoters thus reducing their expression in oral cancer SCC-9 cell line.⁴¹ PTB also showed upregulation of E-cadherin and downregulation of N-Cadherin and epithelial-mesenchymal transition (EMT) markers such as Slug Snail, ZEB1, ZEB2 and vimentin expression thus inhibiting migration and invasion in Hs578t, MCF7 and MDA-MB-231 breast cancer cells and MDA-MB-231 cell tumor xenograft model.⁴² This suppression of EMT status by PTB was produced by suppression of Twist1, vimentin and NFκB and enhancement of E-cadherin levels in both MDA-MB-231 cell xenograft model and M2 TAM-cocultured MCF7 cells lines.^43,44 Moreover, it also decreased MTA1 protein levels leading to suppression of EMT-related tumor metastasis factor vimentin and enhancement of E-cadherin in prostate-specific Pten f/f mouse models of prostate cancer.^37,45 Additionally, PTB also caused inhibition of expression of vascular adhesion molecule 1 in sinusoidal endothelium of hepatic cells thus inhibiting the metastasis by decreasing adhesion of B16M-F10 cell to the endothelium.⁴⁶ Summary of the research outcomes confirmed PTB to be a potent inhibitor of angiogenesis and metastasis.

Antiobesity activity:

PTB has been reported for its antiobesity activity produced through reduction in the activities of lipogenic enzymes in liver and adipose tissue and increase in activities of rate-limiting enzymes of hepatic fatty acid oxidation. PTB also showed its efficacy as delipidating agent in liver steatosis induced Zucker (fa/fa) rats by reducing availability of fatty acids and triacylglycerol synthesis and increasing very fatty acid oxidation and low-density lipoprotein assembly.⁴⁷In another study, PTB produced antiobesity activity through reduction in lipogenesis in adipose tissue by reducing fatty acid synthase and malic enzyme and enhancement of fatty acid oxidation with increased AMPK activity and decreased Acetyl-CoA carboxylase activity. Regulation of lipid metabolism by PTB has been attributed to its PPAR-α agonistic effect.⁴⁸

Antihyperlipidemic activity:

Several studies have shown the advantageous effects of PTB on lipid metabolism in various in vitro and in vivo models. These effects were mainly attributed to regulation of various lipid metabolic molecular pathways through PPAR-α gene induction which is the main target of dyslipidemia therapy.^49,50 It was further confirmed in another study wherein PTB (100μM and 300μM) showed induction of PPAR-α more than standard hypolipidemic drug, ciproﬁbrate in H4IIEC3 cell line.⁵¹ In another study, hypercholesterolemic hamsters fed with PTB (25ppm) produced a 29% decrease in plasma low density lipoprotein (LDL) cholesterol levels and 14% decrease in plasma glucose levels with 7% enhancement in plasma high density lipoprotein (HDL) cholesterol levels, through PPAR-α induction.⁵²Additionally, PTB administration caused downregulation of fatty acid synthase (FAS), PPAR-γ, leptin, resistin, CCAAT/enhancer binding protein (C/EBP)-α while upregulating adiponectin in an adipocyte cell line (3T3L1) model. PTB also exhibited an antiadipogenic action by decreasing triacylglycerol accumulation, cell population growth, and lipid droplet formation in 3T3L1 cells.⁵³ PTB has shown its impact on several genes involved in lipid metabolism causing upregulation of the genes of enzymes involved in fatty acid β-oxidation and metabolism of sphingolipid, phospholipid and sterol. Data concerning PTB and liver steatosis are scarce so far, but the reduction in oxidative stress induced by PTB may be involved since oxidative stress is related to the progression of steatosis to steatohepatitis. Furthermore, PTB caused suppression of lipogenesis by activation of 5′ adenosine monophosphate kinase (AMPK) in adipocytes and human prostate carcinoma cells.^54,55 PTB was able to significantly reduce LDL-cholesterol, serum total cholesterol and triglyceride levels, while elevated HDL-cholesterol in preclinical models of dyslipidemia.⁵⁶ Various investigations have been carried out to evaluate the antiobesity activity of PTB wherein PTB has shown antiobesity effects by increasing fatty acid oxidation and reducing lipogenesis in adipocytes through increase in carnitine acyl-CoA oxidase and palmitoyl-transferase I (CPT-1)A activity in liver.^56,57Additionally, PTB showed significant and dose dependant reduction in total adipose tissue mass in rats. It has also shown reduction in various inﬂammatory biomarkers like IL-6 in 3T3-L1 adipose cells after inﬂammatory reaction by TNF-α.⁵⁶

Another study in insulin resistant rats showed the ability of PTB to increase oxidation of fatty acid in gastrocnemius muscle by enhancing mitochondriogenesis and oxidative capacity of mitochondria by increasing the activities of citrate synthase, CPT-1B, cytochrome c oxidase subunit II and mitochondrial transcription factor A.⁵⁷ Thus the results of different investigations confirmed the usefulness of PTB in treating cardiovascular diseases by virtue of its lipid lowering efficacy.

Antiatherosclerotic activity:

PTB has exhibited various defensive activities against atherosclerosis. Abnormal vascular smooth muscle cells (VSMCs) of arterial blood vessel walls results in atherosclerosis and cardiovascular diseases.^56,57 PTB is shown to exert a marked inhibitory action on DNA synthesis and proliferation of aortic VSMCs of rat.⁵⁸ It also caused concentration dependant reduction in expression regulating factors of cell cycle such as cyclin E, Cdk4, Cdk2, cyclin D1, PCNA and retinoblastoma proteins.⁵⁸ Apart from this, it has counteracted proatherosclerosis induced by oxidized LDL (oxLDL) by modulatory action on autophagy and apoptosis. It also prevented the consequences of autophagy and apoptosis in endothelial cells blood vessels thus preventing proatherosclerosis induced by oxLDL. Antiapoptotic activity was attributed to inhibitory effect of PTB on various mediators of apoptosis such as caspase enzymes, apoptotic proteins, p53 and enhanced effect on cytochrome c and MMP release and by suppressing the expression of lectin like oxLDL receptor-1 (LOX-1).⁵⁹ Attenuation of inﬂammation and oxidative stress, modulation of NF-κB and LOX-1expression are the other important mechanisms of PTB.^59,60Blueberry extract, through its antioxidant activity showed its potency in preventing atherosclerosis by enhancing antioxidant enzymes and reducing markers of oxidative stress in various clinical as well as preclinical studies.^61-67

Cardioprotective activity:

PTB has shown it protective efficacy against cardiovascular diseases in few of investigations. Blueberry rich diet has shown increased myocardial tolerance to ischemic injury as well as reduced myocardial infarct size in coronary artery ligation model in rat.^61-63 It also enhanced survival of cardiomyocytes by increasing the reactive oxygen species threshold of mitochondrial permeability transition, thus inhibiting inﬂammation and necro-apoptosis in ischemic cells.^64-66The ejection fractions were also found to be increased by the extract after two weeks of MI through prolongation of the post MI left ventricular remodeling. PTB has shown its protective effect on rat hearts against ischemia/reperfusion injury with significant reduction in serum and myocardial TNF-α production, infarct size, apoptotic index and myeloperoxidase levels.^67-70 This effect of PTB was attributed to its antiinﬂammatory activity through modulation of toll-like receptor 4/NF-κB signaling pathway, nitric oxide and cGMP signaling pathways.^71,72

Antihypertensive activity:

Antihypertensive activity of PTB has been studied in several preclinical as well as clinical studies. It acts by enhancement of vascular endothelial NOS, inhibition of angiotensin converting enzyme and activation of several antioxidant and protective pathways.^73-77 PTB (250 mg/day), in a clinical study, has shown its efficacy in reducing both systolic and diastolic blood pressure and was found to be safe in normotensive patients.^78-80

Effects on hematologic parameters:

Effect of PTB on several haematological parameters has been extensively investigated. Blueberry supplementation has shown protective activity against oxidative free radical production in RBCs exposed to hydrogen peroxide.^81-83 PTB showed its ability to counteract the 2,2-azobis 2-amidinopropane dihydrochloride induced hemolysis in RBCs with increased GSH levels.^84,85It also inhibited hydrogen peroxide induced lipid peroxidation leading to reduced autoxidation of RBCs showing its protective action on RBCs against oxidative stress by attenuating, the detrimental effects of reactive oxygen species by enhanced hydrogen peroxide scavenging and antioxidant activity.^86-88 Several in vitro as well as in vivo studies reflects the advantageous actions of PTB on macrophages by decreasing the expression of inﬂammatory COX2 and iNOS gene and inactivation of NF-κB, thus inhibiting the activation of proinﬂammatory cytokines towards inﬂammatory stimuli.^89-91PTB has also produced inhibitory effect on prostaglandin E2 production from human blood cells stimulated by lipopolysaccharide in vitro.^92,93 PTB has shown inhibitory action on platelet aggregation induced by collagen and stimulant action on production of platelet nitric oxide by inhibiting generation of platelet reactive oxygen species.^94-96 These effects were attributed to mechanisms such as free radical scavenging in platelets and Akt modulating effect in VSMC exhibiting its efficacy as a potential antithrombotic agent.^97,99

Anti-inflammatory activity:

PTB has been proven for its efficacy in treatment of acute as well as chronic inflammation in several in vivo and in vitro studies such as dermatitis, obesity, neuroinflammation, pancreatitis, atherosclerosis, inﬂammatory bowel disease etc.^100,101 The anti-inflammatory activity has been attributed to several inflammation regulatory mechanisms of PTB upregulation of expression of inhibitory protein nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα), downregulation of expression of nuclear factor kappa B (NF- κ B) signaling, cyclooxygenase-1 and 2, prostaglandin E2(PGE 2) gene, inducible nitric oxide synthase (iNOS), suppression of production of nitric oxide (NO), pro-inﬂammatory cytokines, (IL-6, IL-1 β, IL-8, IL-18 and TNF α) and activation of peroxisome proliferator-activated receptor α (PPAR α )confirmed in various in vitro and in vivo studies.¹⁰³ Decreased COX-2 and iNOS levels were produced by inactivation of NF-κ B or activator protein 1 (AP-1) by PTB by inhibiting the phosphorylation thus stimulating the jun amino-terminal kinase (JNKs), phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), mitogen-activated protein kinase (MAPK) pathways and suppression of p65 nucleus translocation. 33PTB has successfully attenuated inflammation produced by TNF- α, endoplasmic reticulum stress (ERS) signalling as well as HaCaT skin cell inﬂammation induced by potassium dichromate.^104-107

Antiarthritic activity:

PTB has shown positive effects in several arthritic model PTB by various mechanisms such as activation of Nrf2 in cartilage, preventing degeneration of cartilage, protective action on chondrocytes, attenuation of inflammatory mediators such as IL-1β and reactive oxygen species, inhibition of phosphorylation of IκBα and MAPKs (ERK and JNK).¹⁰⁸ PTB was found to reduce neutrophils count showing immunomodulatory effect on arthritis.¹⁰⁹ PTB derivative showed inhibitory effect on osteoclast production in murine macrophages. The results of different studies displayed its usefulness in osteoporosis and other skeletal disorders.¹¹⁰

Antioxidant activity:

Several reports regarding antioxidant potential of PTB have been documented till date. PTB has been proven to enhance plasma antioxidant potential and reduce oxidative stress showing its usefulness in prevention of neurodegenerative diseases, cancer, cardiovascular diseases, diabetes, ischemia, inﬂammatory diseases and pulmonary ﬁbrosis as oxidative stress is a key factor in their pathogenesis.^91-93 It acts by decreased expression of Nrf2, enhancement of antioxidant enzymes levels such as SOD, HO-1, glutathione peroxidase and catalase.⁹⁴ PTB was found to ameliorate early liver injury in intrauterine growth retarded neonates, presumably by stimulating the Nrf2 signals and the associated antioxidant function. It facilitated the nuclear translocation of Nrf2 and promoted the expression levels of SOD-2 in the liver of IUGR piglets.⁹⁵

Miscellaneous:

Piceatannol 4'-β-glucoside showed the strongest inhibitory activity among the stilbene glycosides towards histamine release from rat peritoneal mast cells. Hence, it acts as antiallergic. PTB 4'-β-glucoside showed high phosphodiesterase inhibitory activity.⁹⁶PTB has shown anxiolytic-like actions by down-regulating phosphorylated levels of extracellular regulated kinases in the hippocampus of mice. Unlike resveratrol, PTB anxiolytic-like action was found to be comparable to diazepam at a dose level of 1-2mg/Kg. At higher dose (5 and 10mg/Kg), it did not produce anxiolytic action.⁹⁷ PTB has been found to be more potent than resveratrol in suppressing BaP-mediated airway remodeling and is capable of preventing BaP-associated asthma.⁹⁸ PTB was found to have relatively high antifungal activity than resveratrol and the viniferins. It was found to be toxic to adult mosquito and mosquito larvae. In yet another study, PTB inhibited the germination of Botrytis cinerea conidia and Plasmopara viticola sporangia 5−10 times more effectively than resveratrol.⁹⁹ PTB was found to have the highest anti-androgenic activity among all stilbenoids.¹⁰⁰Pterocarpus marsupium extract and PTB has also been suggested to be useful chronic skin diseases with anti-tyrosinase activities. It improves blood fluidity and brightens dull facial skin.¹¹¹The effect of PTB on endoplasmic reticulum stress and apoptosis in human renal tubular epithelial cells (HK-2 cells) induced by oxalate was studied. The cell viability due to PTB was significantly increased. It has effectively inhibited the endoplasmic reticulum stress and apoptosis of HK-2 cells induced by oxalate.¹¹²PTB has effect on the ability of gram-positive cocci to form biofilm and effectively destroyed pre-formed biofilm in vitro. It is a useful candidate in the treatment of biofilm-associated infections of Staphylococcus and Enterococcus.¹¹³

CONCLUSION:

PTB is widely distributed in Pterocarpus species and in various Vaccinium berries. Its activities have been demonstrated in both preclinical and clinical studies by oral administration. It has anticancer, neuroprotective, antidiabetic, antiobesity, antihyperlipidemic, anti-atherosclerotic, cardioprotective, antihypertensive, anti-inflammatory, anti-arthritic, antioxidant, anti-allergic, anti-anxiety, anti-androgenic and antifungal activity. Exhaustive study described its usefulness as an anticancer agent.

CONFLICT OF INTEREST:

The authors have no conflicts of interest regarding this investigation.

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Received on 14.07.2021 Modified on 09.12.2022

Research J. Pharm. and Tech 2023; 16(11):5514-5521.

DOI: 10.52711/0974-360X.2023.00892