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Updated: Mar 11, 2026
Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome
Published on: July 5, 2024
Protective Effect of "Ark-e-Kasni," a Unani Formulation, in Letrozole and High-Fat Diet-Induced Polycystic Ovarian
Kamini R Shirasath1, Ritu Karwasra2, N Zaheer Ahmed2
1Department of Pharmacology, Shri Vile Parle Kelavani Mandal's Institute of Pharmacy, Dhule, Maharashtra, India.
Aim:
The present study aimed to evaluate the therapeutic potential of the Unani formulation Ark-e-Kasni in alleviating the symptoms of polycystic ovary syndrome (PCOS).
Methods:
In the present study, letrozole and a high-fat diet (HFD) were used to induce PCOS-like symptoms in rats. After induction, different groups were treated with varying doses of Ark-e-Kasni (5, 10, and 20 mL/kg), metformin, and finasteride. At the end of treatment, blood and ovaries were collected for biochemical and histological analysis.
Results:
A significant weight gain and prolonged diestrous phase were observed in PCOS rats, accompanied by a considerable elevation in LH (42.52 ± 0.90 mIU/mL) and testosterone (8370 ± 122.18 pg/mL), and a low level of FSH (11.86 ± 0.43 mIU/mL). Moreover, an increase in insulin (14.31 ± 0.35 mIU/mL), TNF-α (358.81 ± 9.81 pg/mL), IL-1β (143.74 ± 3.39 pg/mL), and IL-6 (154.04 ± 2.04 pg/mL), and a reduction in SOD, CAT, and GSH were noticed. While the Ark-e-Kasni restored the levels of LH (30.97 ± 1.04 mIU/mL), testosterone (5651.83 ± 182.69 pg/mL), FSH (15.66 ± 0.56 mIU/mL), insulin (5.48 ± 0.23 mIU/mL), TNF-α (212.16 ± 8.66 pg/mL), IL-1β (78.79 ± 1.46 pg/mL), and IL-6 (74.53 ± 1.60 pg/mL), and lipid markers. Histological and microscopic analysis showed reduced cystic follicles and enhanced corpus luteum formation, improving ovarian morphology.
Conclusion:
The findings suggest that Ark-e-Kasni ameliorates PCOS through diverse molecular mechanisms. Ark-e-Kasni may modulate steroidogenic enzyme activity to reduce hyperandrogenism, enhance insulin sensitivity through the PI3K/Akt pathway, and inhibit the downstream inflammatory pathway of NF-κB.
