Karanjin Author Singh, A. Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Assam, 781039, India Author Bhatt, G. Author Gujre, N. Author Mitra, S. Author Swaminathan, R. Author Limaye, A. M. Author Rangan, L. text Phytochemistry 2021 112641 2021-03-31 183 1 13 http://dx.doi.org/10.1016/j.phytochem.2020.112641 journal article 264548 10.1016/j.phytochem.2020.112641 5ca76737-bf9d-472b-87d5-6d98a5ae7f66 1873-3700 8291563

Table 2 In vitro studies of pharmacological effects of karanjin.

S.	Cell line	Pharmacological	Methods	Result obtained	IC50 after 24 h (μM)	Reference
AKT - Protein kinase B; AMPK - 5 ′ adenosine monophosphate-activated protein kinase; CYP - Cytochromes P450; ERODE - 7-ethoxy-resorufin-O-deethylase; FITC - Fluorescein isothiocyanate; MTT - (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide); NF-κB - Nuclear factor kappa B; PTPase-1β - Protein tyrosine phosphatase 1β; ROS - Reactive oxygen species.
No		Effect
1	L6-GLUT4 myc cells	Anti-diabetic	a. Muscles cells over-expressing	a. Significant karanjin stimulated	25	Jaiswal
			GLUT4 myc tag were treated with	GLUT4 translocation was		et al.
			different doses of karanjin.	demonstrated at 10 μM, reaching a		(2011)
				maximal level at 25 μM (1.9-fold).
			b. PTPase activity was also	b. Karanjin treatment had no
			determined in L6-GLUT4 myc	significant effect on cell viability as
			myotubes following treatment with	assessed by MTT assay and protein
			karanjin for 16 h.	measurement.
				c. Karanjin inhibited the activity of
				PTPase in a dose-dependent manner
				with percent inhibition of 10.8 and
				21.2 at 10 and 25 μM concentrations,
				respectively.
				d. Karanjin-induced mechanism
				enhanced glucose uptake due to
				increased translocation of GLUT4 to
				plasma membrane-associated with
				activation of AMPK pathway, in a PI
				3-kinase/AKT-independent manner.
2	Human lung adenocarcinoma	Anti-cancer	a. The inhibition of cell growth by	a. Cell cycle was markedly blocked at	35.3 (A549), 7.2	Guo et al.
	(A549), human hepatocellular		karanjin was investigated via the	G2/M phase in A549, moderately	(HEPG2), and 10	(2015)
	carcinoma (HEPG2), and		MTT assay.	perturbed in HL-60, and least	(HL-60)
	human acute promyelocytic			arrested in HepG2 upon karanjin
	leukemia (HL-60)			treatment.
			b. Lung adenocarcinoma cells are	b. Karanjin caused inhibition of cell
			treated with different doses of	proliferation by increased cell
			karanjin for 72 h.	apoptosis.
			c. Apoptosis was quantified by the
			Annexin V-FITC assay and analyzed
			by flow cytometry.
3	Human kidney cells (CYP-	Metabolism	a. Karanjin at different	a. Karanjin demonstrated the high	0.03 (CYP1A1),	Joshi et al.
	expressing-HEK293)		concentrations was screened for	percentage inhibition of the CYP1A1	0.01 (CYP 1A2),	(2018)
			CYP1A1-enzyme inhibition activity	enzyme and IC50 of 1.6 μM in EROD	and 0.22 (CYP 1B1)
			using sacchrosomes™ by the EROD	assay and IC50 of 30 nM in CYP1A1
			assay. b. Transiently transfected	overexpressing HEK293 cells. b.
			recombinant HEK293	Karanjin also showed to protect the
			overexpressing CYP1A1 cells were	adherent CYP1A1-expressing
			incubated with different	HEK293 cells from benzo [a]pyrene
			concentrations of karanjin for 30	mediated toxicity, thereby,
			min for the determination of IC50	indicating its potential to interfere
			values.	with the metabolism of pro-
				carcinogens to active carcinogens
				and act as a chemopreventive agent.
4	Human cervical cancer cells	Non-toxic	Cells were treated with different	a. Karanjin inhibited HeLa cell	186 (HeLa) and 86	Raghav
	(HeLa) and mouse fibroblast		concentrations of karanjin (0–200	proliferation by 7.4, 13, 17, 23, 27,	(L929)	et al.
	cells (L929)		μM).	and 48% at 20, 40, 60, 80, 100 and		(2019)
				180 μM, respectively. b. Karanjin
				inhibited L929 cells proliferation by
				27, 31, 43, 53, 61, and 70% at 10, 20,
				50, 100, 150, and 200 μM,
				respectively.
5	Breast carcinoma cell line	Non-toxic	Cytotoxicity assay, intracellular ROS	a. Karanjin could decrease ROS level	160.97–215.37	Roy et al.
	(MDA MB-231), Lung		level, DNA damage measurement,	by inhibition of I-κB degradation		(2019)
	carcinoma (NCI–H460),		and analysis of cell cycle were	resulting in restriction of NF-κB
	Cervical cancer (HeLa), and		performed and analyzed upon	nuclear translocation. b. Karanjin
	Hepatocellular carcinoma		treatment with karanjin (0–100 μg	Induced BAX/BCL-2 ratio by
	(Hep-G2)		ml 1).	inhibiting BCL-2 expression. c.
				Karanjin treatment showed low DNA
				damage with increased p53
				expression.
6	Human breast cancer cells	Anti-tumor	Breast cancer cells were treated with	Karanjin could significantly inhibit	11.66 (MCF-7) and	Mrudul
	(MCF-7 and MDAMD-231)		karanjin at different concentrations	cell proliferation in MCF-7 cells,	18.56 (MDAMD-	et al.
			(0, 2.5, 5, 10, 20, and 40 μM).	indicating its potential to be used as	231)	(2020)
				an anti-cancer agent.